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1. Toyoda T, Kamei Y, Kato H, Sugita S, Takeya M, Suganami T, Ogawa Y: Effect of peroxisome proliferator-activated receptor-alpha ligands in the interaction between adipocytes and macrophages in obese adipose tissue. Obesity (Silver Spring); 2008 Jun;16(6):1199-207
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  • [Title] Effect of peroxisome proliferator-activated receptor-alpha ligands in the interaction between adipocytes and macrophages in obese adipose tissue.
  • OBJECTIVE: This study was designed to examine the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligands on the inflammatory changes induced by the interaction between adipocytes and macrophages in obese adipose tissue.
  • METHODS AND PROCEDURES: PPAR-alpha ligands (Wy-14,643 and fenofibrate) were added to 3T3-L1 adipocytes, RAW264 macrophages, or co-culture of 3T3-L1 adipocytes and RAW264 macrophages in vitro, and monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) mRNA expression and secretion were examined.
  • PPAR-alpha ligands were administered to genetically obese ob/ob mice for 2 weeks.
  • Moreover, the effect of PPAR-alpha ligands was also evaluated in the adipose tissue explants and peritoneal macrophages obtained from PPAR-alpha-deficient mice.
  • RESULTS: In the co-culture of 3T3-L1 adipocytes and RAW264 macrophages, PPAR-alpha ligands reduced MCP-1 and TNF-alpha mRNA expression and secretion in vitro relative to vehicle-treated group.
  • The anti-inflammatory effect of Wy-14,643 was observed in adipocytes treated with macrophage-conditioned media or mouse recombinant TNF-alpha and in macrophages treated with adipocyte-conditioned media or palmitate.
  • Systemic administration of PPAR-alpha ligands inhibited the inflammatory changes in adipose tissue from ob/ob mice.
  • Wy-14,643 also exerted an anti-inflammatory effect in the adipose tissue explants but not in peritoneal macrophages obtained from PPAR-alpha-deficient mice.
  • DISCUSSION: This study provides evidence for the anti-inflammatory effect of PPAR-alpha ligands in the interaction between adipocytes and macrophages in obese adipose tissue, thereby improving the dysregulation of adipocytokine production and obesity-related metabolic syndrome.
  • [MeSH-major] Adipocytes / drug effects. Cell Communication / drug effects. Fenofibrate / pharmacology. Macrophages / drug effects. Obesity / metabolism. PPAR alpha / metabolism. Pyrimidines / pharmacology
  • [MeSH-minor] 3T3-L1 Cells. Animals. Anti-Inflammatory Agents / pharmacology. Cell Line. Chemokine CCL2 / metabolism. Coculture Techniques. Disease Models, Animal. Ligands. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Obese. Peritoneal Cavity / pathology. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18356826.001).
  • [ISSN] 1930-7381
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Ligands; 0 / PPAR alpha; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 86C4MRT55A / pirinixic acid; U202363UOS / Fenofibrate
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2. Li B, Shi M, Li J, Zhang H, Chen B, Chen L, Gao W, Giuliani N, Zhao RC: Elevated tumor necrosis factor-alpha suppresses TAZ expression and impairs osteogenic potential of Flk-1+ mesenchymal stem cells in patients with multiple myeloma. Stem Cells Dev; 2007 Dec;16(6):921-30
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  • [Title] Elevated tumor necrosis factor-alpha suppresses TAZ expression and impairs osteogenic potential of Flk-1+ mesenchymal stem cells in patients with multiple myeloma.
  • Because TAZ, a Runx2/Cbfa1 transcriptional co-activator, has recently been shown to modulate mesenchymal stem cell (MSC) differentiation in favor of osteoblast differentiation, we investigated whether the regulation of TAZ expression played a role in the decreased bone formation of MM.
  • We isolated and purified Flk-1(+)CD31(-)CD34(-) cells with MSC characters from bone marrow (BM) of myeloma patients and healthy donors.
  • We found the osteogenic potential of the MSCs from myeloma patients decreased significantly, and TAZ expression of these cells was lower than that of healthy donors.
  • Human myeloma cell lines (HMCLs) and CD138(+) myeloma cells (MCs) from myeloma patients inhibited osteogenesis of the MSCs from healthy volunteers, which were accompanied by a reduced TAZ expression and elevated TNF-alpha concentration in the supernatant of co-culture systems.
  • The repressed osteogenesis and TAZ expression were both partially restored by neutralization of TNF-alpha.
  • Thus, the decreased osteogenic potential of MSCs of myeloma patients was in part due to TNF-alpha suppressed TAZ expression.
  • [MeSH-major] Gene Expression Regulation / drug effects. Mesenchymal Stromal Cells / pathology. Mesenchymal Stromal Cells / physiology. Multiple Myeloma / physiopathology. Osteogenesis / drug effects. Proteins / genetics. Transcription Factors / genetics. Tumor Necrosis Factor-alpha / pharmacology. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Coculture Techniques. Female. Humans. Karyotyping. Male. Middle Aged. Osteoblasts / cytology. Osteoblasts / pathology. Reference Values. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17927494.001).
  • [ISSN] 1547-3287
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / TAZ protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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3. Spaeth EL, Dembinski JL, Sasser AK, Watson K, Klopp A, Hall B, Andreeff M, Marini F: Mesenchymal stem cell transition to tumor-associated fibroblasts contributes to fibrovascular network expansion and tumor progression. PLoS One; 2009;4(4):e4992
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  • [Title] Mesenchymal stem cell transition to tumor-associated fibroblasts contributes to fibrovascular network expansion and tumor progression.
  • BACKGROUND: Tumor associated fibroblasts (TAF), are essential for tumor progression providing both a functional and structural supportive environment.
  • TAF, known as activated fibroblasts, have an established biological impact on tumorigenesis as matrix synthesizing or matrix degrading cells, contractile cells, and even blood vessel associated cells.
  • The production of growth factors, cytokines, chemokines, matrix-degrading enzymes, and immunomodulatory mechanisms by these cells augment tumor progression by providing a suitable environment.
  • There are several suggested origins of the TAF including tissue-resident, circulating, and epithelial-to-mesenchymal-transitioned cells.
  • METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that TAF are derived from mesenchymal stem cells (MSC) that acquire a TAF phenotype following exposure to or systemic recruitment into adenocarcinoma xenograft models including breast, pancreatic, and ovarian.
  • 3) production of pro-tumorigenic growth factors including hepatocyte growth factor, epidermal growth factor, and interleukin-6; and 4) factors indicative of vascularization, including alpha-smooth muscle actin, desmin, and vascular endothelial growth factor.
  • We demonstrate that under long-term tumor conditioning in vitro, MSC express TAF-like proteins.
  • Additionally, human MSC but not murine MSC stimulated tumor growth primarily through the paracrine production of secreted IL6.
  • CONCLUSIONS/SIGNIFICANCE: Our results suggest the dependence of in vitro Skov-3 tumor cell proliferation is due to the presence of tumor-stimulated MSC secreted IL6.
  • The subsequent TAF phenotype arises from the MSC which ultimately promotes tumor growth through the contribution of microvascularization, stromal networks, and the production of tumor-stimulating paracrine factors.

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  • [ErratumIn] PLoS One. 2013; 8(3). doi:10.1371/annotation/4ab4c130-16cb-41f0-9507-b00ce070fbc6
  • (PMID = 19352430.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA-109451; United States / NCI NIH HHS / CA / R01 CA109451; United States / NCI NIH HHS / CA / RC1 CA146381; United States / NCI NIH HHS / CA / P50 CA116199; United States / NCI NIH HHS / CA / CA-49639; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / BC / BC083397; United States / NCI NIH HHS / CA / CA-116199; United States / NCI NIH HHS / CA / CA-55164; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2661372
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4. Singh RR, Barnes CJ, Talukder AH, Fuqua SA, Kumar R: Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein. Cancer Res; 2005 Nov 15;65(22):10594-601
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  • [Title] Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein.
  • Here, we have identified estrogen receptor alpha (ERalpha) and its corepressor, metastasis tumor antigen 1 (MTA1), as two novel binding partners of LMO4.
  • These findings suggested that LMO4 was an integral part of the molecular machinery involved in the negative regulation of ERalpha transactivation function in breast cells.
  • Because LMO4 is up-regulated in human breast cancers, repression of ERalpha transactivation functions by LMO4 might contribute to the process of breast cancer progression by allowing the development of ERalpha-negative phenotypes, leading to increased aggressiveness of breast cancer cells.
  • [MeSH-major] Estrogen Receptor alpha / physiology. Homeodomain Proteins / metabolism. Transcription Factors / metabolism. Transcriptional Activation / physiology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Cell Line, Tumor. Chromatin / genetics. Chromatin / metabolism. Estrogen Receptor beta / metabolism. Gene Expression Regulation, Neoplastic / physiology. Histone Deacetylases / metabolism. Humans. LIM Domain Proteins. Repressor Proteins / metabolism

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  • (PMID = 16288053.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098823; United States / NCI NIH HHS / CA / CA90970
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromatin; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / LMO4 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
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5. Ohta H, Hamada J, Tada M, Aoyama T, Furuuchi K, Takahashi Y, Totsuka Y, Moriuchi T: HOXD3-overexpression increases integrin alpha v beta 3 expression and deprives E-cadherin while it enhances cell motility in A549 cells. Clin Exp Metastasis; 2006;23(7-8):381-90
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  • [Title] HOXD3-overexpression increases integrin alpha v beta 3 expression and deprives E-cadherin while it enhances cell motility in A549 cells.
  • We have previously shown that transduction of HOXD3, one of homeobox genes, into human lung cancer A549 cells enhances cell motility, invasion and metastasis.
  • In the present study, we examined the roles of integrin beta3 which was up-regulated by HOXD3-overexpression in the HOXD3-induced motility of A549 cells.
  • We first established integrin beta3-transfectants and compared their motile activity to those of the HOXD3-transfected, control-transfected and parental cells by three different assays.
  • The integrin beta3-transfectants as well as the HOXD3-transfectants formed heterodimer with integrin alphav subunit, and showed highly motile activities assessed by haptotaxis or phagokinetic track assay compared to the control transfectants or parental cells.
  • In vitro wound-healing assay revealed that migratory activities were graded as the HOXD3-transfectants > the integrin beta3-transfectants > the control transfectants or parental cells.
  • An addition of function-blocking antibody to E-cadherin into the wound-healing assay promoted the migratory activity of the integrin beta3-transfectants, suggesting that E-cadherin prevented the cells from dissociating from the wound edges.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement. Humans. Mice. Neoplasm Metastasis. Signal Transduction. Transforming Growth Factor beta / pharmacology. Wound Healing

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  • (PMID = 17187229.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Integrin alphaVbeta3; 0 / Transforming Growth Factor beta; 127609-92-1 / HOXA4 protein, human
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6. Scheim DE: Cytotoxicity of unsaturated fatty acids in fresh human tumor explants: concentration thresholds and implications for clinical efficacy. Lipids Health Dis; 2009;8:54
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  • [Title] Cytotoxicity of unsaturated fatty acids in fresh human tumor explants: concentration thresholds and implications for clinical efficacy.
  • BACKGROUND: Unsaturated fatty acids (UFAs) exhibit in vitro cytotoxicity against many malignant cell lines and yield decreased cancer incidence and reduced tumor growth in animal models.
  • To explore possibilities for enhanced clinical efficacy, fresh surgical explants of tumors from 22 patients with five malignancies were exposed to gamma-linolenic acid (GLA) and alpha-linolenic acid (ALA) and analyzed with an in vitro chemosensitivity testing system, the Fluorescent Cytoprint Assay (FCA).
  • A total of 282 micro-organ cultures derived from these malignant tumors were exposed to GLA and ALA at different concentrations.
  • In tests using 30-40% serum, GLA and ALA killed tumor at concentrations of 2 mM and above.
  • CONCLUSIONS: The concentration threshold of 500 microM to 2 mM exhibited for antitumor activity by GLA and ALA is much higher than that observed in most previously reported cell culture studies but consistent with physiological concentrations found to kill tumor clinically and in animals.
  • [MeSH-major] Neoplasms / pathology. alpha-Linolenic Acid / pharmacology. gamma-Linolenic Acid / pharmacology
  • [MeSH-minor] Cell Death / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Serum. Treatment Outcome

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  • (PMID = 20003514.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0RBV727H71 / alpha-Linolenic Acid; 78YC2MAX4O / gamma-Linolenic Acid
  • [Other-IDs] NLM/ PMC2801488
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7. Buck I, Morceau F, Cristofanon S, Heintz C, Chateauvieux S, Reuter S, Dicato M, Diederich M: Tumor necrosis factor alpha inhibits erythroid differentiation in human erythropoietin-dependent cells involving p38 MAPK pathway, GATA-1 and FOG-1 downregulation and GATA-2 upregulation. Biochem Pharmacol; 2008 Nov 15;76(10):1229-39
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  • [Title] Tumor necrosis factor alpha inhibits erythroid differentiation in human erythropoietin-dependent cells involving p38 MAPK pathway, GATA-1 and FOG-1 downregulation and GATA-2 upregulation.
  • The proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) has been linked to inflammation- and cancer-related anemia, which reduces both quality of life and prognosis of patients.
  • These changes led to an inhibition of erythroid gene expression including Epo receptor (EpoR), alpha- and gamma-globin, erythroid-associated factor (ERAF), hydroxymethylbilane synthetase (HMBS), and glycophorin A (GPA).
  • Indeed the p38 inhibitor, SB203580, abrogated the inhibitory effect of TNFalpha on the major erythroid transcription factor GATA-1 as well as erythroid marker expression in Epo-induced TF-1 cells.
  • [MeSH-major] Erythropoiesis / physiology. GATA1 Transcription Factor / metabolism. GATA2 Transcription Factor / biosynthesis. Nuclear Proteins / metabolism. Transcription Factors / metabolism. Tumor Necrosis Factor-alpha / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Differentiation / physiology. Cell Line, Tumor. Down-Regulation / drug effects. Down-Regulation / physiology. Erythropoietin / genetics. Erythropoietin / metabolism. Humans. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / metabolism. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Up-Regulation / drug effects. Up-Regulation / physiology

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  • (PMID = 18805401.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / ZFPM1 protein, human; 11096-26-7 / Erythropoietin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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8. Tennant DA, Gottlieb E: HIF prolyl hydroxylase-3 mediates alpha-ketoglutarate-induced apoptosis and tumor suppression. J Mol Med (Berl); 2010 Aug;88(8):839-49
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  • [Title] HIF prolyl hydroxylase-3 mediates alpha-ketoglutarate-induced apoptosis and tumor suppression.
  • Many solid tumors consist of large regions of poorly perfused cells, resulting in areas of low oxygen (hypoxia) throughout the cell mass.
  • Cells subjected to hypoxia turn on a complex set of responses that alter their metabolism, rebalance their survival mechanisms, increase their invasive capacity, and stimulate angiogenesis.
  • This allows them to at least temporarily escape the nutrient starvation and cell death resulting from this hostile environment.
  • Accordingly, the hypoxic regions of tumors are often sources of the most aggressive and therapy-resistant cells, and therefore those cells that drive tumorigenesis.
  • The hypoxia inducible factor (HIF) prolyl hydroxylases (PHDs) are enzymes that are functionally inactivated in hypoxia, as they use both oxygen and alpha-ketoglutarate as substrates to hydroxylate target prolyl residues.
  • Although HIF1alpha, the most highly characterized PHD target, orchestrates many of the cellular responses to hypoxia observed in tumors, PHDs themselves have previously been shown to regulate some hypoxia responses, including apoptosis, in a HIF-independent mechanism.
  • This led us to investigate whether chronic reactivation of these enzymes may inhibit tumor progression.
  • We show here that esterified alpha-ketoglutarate given daily will induce apoptosis and inhibit tumor growth, in vivo.
  • These data suggest that PHD3 may be a valid target in vivo for anti-tumor therapy.
  • [MeSH-minor] Animals. Cell Hypoxia. Cell Line, Tumor. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor-Proline Dioxygenases. Mice. Mice, Nude

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  • (PMID = 20383689.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ketoglutaric Acids; 8ID597Z82X / alpha-ketoglutaric acid; EC 1.13.11.- / Dioxygenases; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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9. Singhatanadgit W, Salih V, Olsen I: Bone morphogenetic protein receptors and bone morphogenetic protein signaling are controlled by tumor necrosis factor-alpha in human bone cells. Int J Biochem Cell Biol; 2006;38(10):1794-807
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  • [Title] Bone morphogenetic protein receptors and bone morphogenetic protein signaling are controlled by tumor necrosis factor-alpha in human bone cells.
  • Bone morphogenetic proteins (BMP) stimulate osteoblast differentiation by signal transduction via three BMP receptors (BMPR-IA, -IB and -II), whereas the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) has been shown to suppress osteoblast differentiation.
  • Although the mechanisms which regulate the BMPR are not yet known, it is possible that they may be negatively controlled by TNF-alpha, thereby inhibiting BMP-induced osteoblast differentiation.
  • To test this hypothesis, we have examined the effects of TNF-alpha on BMPR-IA, -IB and -II expression and the functional consequences of this cytokine on BMPR-mediated functions in human bone cells.
  • The results showed that although TNF-alpha down-regulated BMPR-IA and -II transcripts, it increased the level of BMPR-IB mRNA via a MAPK-dependent pathway.
  • In marked contrast, however, TNF-alpha nevertheless caused marked down-regulation of the expression of the BMPR-IB surface antigen specifically.
  • Moreover, the cytokine-induced decrease in BMPR-IB expression was found to be associated with the concurrent presence of a 'soluble' form of this antigen in supernatants of TNF-alpha-treated cultures.
  • Furthermore, the TNF-alpha-induced loss of BMPR-IB was found to ablate BMP-2-stimulated bone cell functions, including phosphorylation of Smad1/5/8, alkaline phosphatase activity and osteocalcin expression.
  • In conclusion, our study has provided evidence, for the first time, that BMPR can be differentially modulated by TNF-alpha at both the post-transcriptional and post-translational levels, with the TNF-alpha-induced shedding of the BMPR-IB antigen associated with a significantly diminished response to BMP-2 in vitro.
  • [MeSH-major] Bone Morphogenetic Protein Receptors / metabolism. Bone and Bones / drug effects. Gene Expression Regulation. Osteoclasts / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antigens / analysis. Antigens / genetics. Antigens / metabolism. Bone Morphogenetic Protein 2. Bone Morphogenetic Proteins / pharmacology. Cell Differentiation / drug effects. Cells, Cultured. Down-Regulation. Humans. Mitogen-Activated Protein Kinase Kinases / metabolism. Osteocytes / chemistry. Osteocytes / drug effects. Osteocytes / metabolism. Phosphorylation. Protein Biosynthesis / drug effects. Signal Transduction. Transcription, Genetic / drug effects. Transforming Growth Factor beta / pharmacology. Ubiquitin-Protein Ligases / metabolism

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  • (PMID = 16797218.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / BMP2 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 6.3.2.19 / SMURF1 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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10. Ding YH, Mrizek M, Lai Q, Wu Y, Reyes R Jr, Li J, Davis WW, Ding Y: Exercise preconditioning reduces brain damage and inhibits TNF-alpha receptor expression after hypoxia/reoxygenation: an in vivo and in vitro study. Curr Neurovasc Res; 2006 Nov;3(4):263-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exercise preconditioning reduces brain damage and inhibits TNF-alpha receptor expression after hypoxia/reoxygenation: an in vivo and in vitro study.
  • We investigated whether gradual increases in tumor necrosis factor-alpha (TNF-alpha) reported during exercise down-regulates expression of TNF-alpha receptors I and II (TNFRI and II) in stroke, leading to reduced brain damage.
  • Spatial distribution of TNF-alpha receptors in brain regions was determined with immunocytochemistry.
  • In human umbilical vein endothelial cells (HUVEC), we addressed the causal effect of TNF-alpha pretreatment on TNF I and II expression using ELISA and real-time PCR.
  • The TNF-alpha receptors were restricted to the ischemic core.
  • An in vitro study revealed a causal link between TNF-alpha pretreatment and reduced cellular expression of TNF-alpha receptors under hypoxic/reoxygenated conditions.
  • Our results suggest that reduced-brain damage in ischemic rats after exercise preconditioning may be attributable to the reduced expression of TNF-alpha receptors.
  • Chronically increased TNF-alpha expression was also found to reduce TNFI and II responding to acute ischemia/reperfusion insult.
  • [MeSH-major] Exercise Therapy / methods. Hypoxia, Brain / prevention & control. Physical Conditioning, Animal / physiology. Reperfusion Injury / rehabilitation. Stroke / rehabilitation. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Disease Models, Animal. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Exercise Test. Humans. Infarction, Middle Cerebral Artery / metabolism. Infarction, Middle Cerebral Artery / physiopathology. Infarction, Middle Cerebral Artery / rehabilitation. Male. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Tumor Necrosis Factor, Type I / agonists. Receptors, Tumor Necrosis Factor, Type I / genetics. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / agonists. Receptors, Tumor Necrosis Factor, Type II / genetics. Receptors, Tumor Necrosis Factor, Type II / metabolism. Recovery of Function / drug effects. Recovery of Function / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Treatment Outcome

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  • (PMID = 17109621.001).
  • [ISSN] 1567-2026
  • [Journal-full-title] Current neurovascular research
  • [ISO-abbreviation] Curr Neurovasc Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
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11. Park KG, Lee KM, Chang YC, Magae J, Ando K, Kim KB, Kim YN, Kim HS, Park JY, Lee KU, Lee IK: The ascochlorin derivative, AS-6, inhibits TNF-alpha-induced adhesion molecule and chemokine expression in rat vascular smooth muscle cells. Life Sci; 2006 Dec 14;80(2):120-6
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  • [Title] The ascochlorin derivative, AS-6, inhibits TNF-alpha-induced adhesion molecule and chemokine expression in rat vascular smooth muscle cells.
  • Herein we examine the effects of a newly identified synthetic PPARgamma ligand, ascochlorin-6 (AS-6), on TNF-alpha-stimulated NF-kappaB activity and inflammatory molecule expression in vascular smooth muscle cells (VSMCs).
  • AS-6 successfully inhibited TNF-alpha-stimulated NF-kappaB activity and inflammatory molecule expression, including vascular cell adhesion molecule-1 (VCAM-1), monocyte chemotactic protein-1 (MCP-1), and fractalkine (CX3CL1).
  • Transient transfection with an [NF-kappaB]x4 luciferase reporter construct showed that AS-6 inhibition of TNF-alpha-stimulated NF-kappaB activation was PPARgamma-dependent.
  • The effects of AS-6 on TNF-alpha-stimulated VCAM-1 and CX3CL1 expression were abolished in cells transfected with an adenovirus expressing dominant-negative PPARgamma and in cells treated with a PPARgamma specific inhibitor, GW9662, confirming again that the anti-inflammatory effect of AS-6 was PPARgamma-dependent.
  • The inhibitory effects of AS-6 on TNF-alpha-stimulated inflammatory gene expression and NF-kappaB activation were more potent than those of rosiglitazone and pioglitazone.
  • This study shows that AS-6 reduces the inflammatory response to TNF-alpha in VSMCs.
  • [MeSH-major] Alkenes / chemistry. Chemokines, CX3C / biosynthesis. Glycolates / pharmacology. Membrane Proteins / biosynthesis. Muscle, Smooth, Vascular / cytology. PPAR gamma / metabolism. Phenols / chemistry. Tumor Necrosis Factor-alpha / pharmacology. Vascular Cell Adhesion Molecule-1 / biosynthesis
  • [MeSH-minor] Adenoviridae / genetics. Animals. Aorta, Thoracic / cytology. Blotting, Northern. Blotting, Western. Cells, Cultured. Chemokine CCL2 / metabolism. Chemokine CX3CL1. Gene Expression / drug effects. Genetic Vectors. Ligands. Male. NF-kappa B / metabolism. Rats. Rats, Sprague-Dawley. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 16989870.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkenes; 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Chemokine CX3CL1; 0 / Chemokines, CX3C; 0 / Cx3cl1 protein, rat; 0 / Glycolates; 0 / Ligands; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / PPAR gamma; 0 / Phenols; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 0 / ascochlorin; 84435-25-6 / 4-O-carboxymethylascochlorin
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12. Grant-Tschudy KS, Wira CR: Hepatocyte growth factor regulation of uterine epithelial cell transepithelial resistance and tumor necrosis factor alpha release in culture. Biol Reprod; 2005 Apr;72(4):814-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatocyte growth factor regulation of uterine epithelial cell transepithelial resistance and tumor necrosis factor alpha release in culture.
  • Underlying stromal cells are essential for the normal development of epithelial cells (ECs) at mucosal surfaces.
  • Recent studies from our laboratory have shown that uterine stromal cells regulate EC integrity, measured as transepithelial resistance (TER) as well as tumor necrosis factor (TNF) alpha alpha secretion by ECs in culture.
  • Using stromal cells in coculture with polarized ECs grown on inserts, we found that stromal cells produce soluble mediators that increase TER and decrease TNFalpha secretion.
  • The purpose of the present study was to identify the mechanisms whereby stromal cells exert their effects on uterine epithelium.
  • When ECs and/or stromal cells were incubated with anti-HGF or anti-HGF receptor (HGFR) antibody before HGF, the effects of HGF were blocked.
  • Neutralization of stromal cell secretions with antibodies for HGF and HGFR demonstrate that stromal-derived HGF is the mediator of EC TER.
  • In contrast, neither anti-HGF antibody nor HGFR antibody had any effect on stromal cell-induced decreases in TNFalpha secretion.
  • From these results, we conclude that stromal cell regulation of EC TER is mediated through the secretion of stromal HGF.
  • [MeSH-major] Epithelial Cells / metabolism. Hepatocyte Growth Factor / pharmacology. Tumor Necrosis Factor-alpha / metabolism. Uterus / cytology. Uterus / metabolism
  • [MeSH-minor] Animals. Antibodies / pharmacology. Cell Polarity / physiology. Cells, Cultured. Coculture Techniques. Electric Impedance. Female. Mice. Mice, Inbred BALB C. Signal Transduction / drug effects. Signal Transduction / physiology. Stromal Cells / cytology. Stromal Cells / drug effects. Stromal Cells / metabolism. Tight Junctions / metabolism

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  • (PMID = 15576826.001).
  • [ISSN] 0006-3363
  • [Journal-full-title] Biology of reproduction
  • [ISO-abbreviation] Biol. Reprod.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-13541
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Tumor Necrosis Factor-alpha; 67256-21-7 / Hepatocyte Growth Factor
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13. Alotaibi H, Yaman EC, Demirpençe E, Tazebay UH: Unliganded estrogen receptor-alpha activates transcription of the mammary gland Na+/I- symporter gene. Biochem Biophys Res Commun; 2006 Jul 14;345(4):1487-96
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  • [Title] Unliganded estrogen receptor-alpha activates transcription of the mammary gland Na+/I- symporter gene.
  • The function of sodium iodide symporter (Na(+)/I(-) symporter, or NIS) in mammary epithelial cells is essential for the accumulation of I(-) in milk; the newborn's first source of I(-) for thyroid hormone synthesis.
  • In this study, using breast cancer cell lines, we established that tRA-responsive NIS expression is confined to estrogen receptor-alpha (ERalpha) positive cells and we investigated the role of ERalpha in the regulation of NIS expression.
  • We showed that the suppression of endogenous ERalpha by RNA interference downregulates NIS expression in ERalpha positive mammary cells.
  • Besides, in an ERalpha negative cell line, reintroduction of ERalpha resulted in the expression of NIS in a ligand-independent manner.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Symporters / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Base Sequence. Blotting, Western. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Gene Expression / drug effects. Humans. Ligands. Molecular Sequence Data. Promoter Regions, Genetic / genetics. RNA Interference. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Response Elements / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tretinoin / pharmacology

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  • (PMID = 16730657.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Ligands; 0 / Receptors, Retinoic Acid; 0 / Symporters; 0 / retinoic acid receptor alpha; 0 / sodium-iodide symporter; 5688UTC01R / Tretinoin
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14. Yang X, Chu Y, Wang Y, Guo Q, Xiong S: Vaccination with IFN-inducible T cell alpha chemoattractant (ITAC) gene-modified tumor cell attenuates disseminated metastases of circulating tumor cells. Vaccine; 2006 Apr 5;24(15):2966-74
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  • [Title] Vaccination with IFN-inducible T cell alpha chemoattractant (ITAC) gene-modified tumor cell attenuates disseminated metastases of circulating tumor cells.
  • IFN-inducible T cell alpha chemoattractant (ITAC) has been demonstrated to be able to induce Th1-type immune response.
  • However, the effects of ITAC on the tumor metastasis have not been fully understood.
  • In the present study, the ITAC-modified tumor cell vaccine in inhibiting the disseminated pulmonary metastasis was evaluated.
  • ITAC-modified tumor cell vaccine 4T1-ITAC was developed by stably transfecting 4T1 cells with pcDNA3-ITAC plasmid.
  • The number of clonogenic metastatic tumor cells and metastatic forci on the surface of lung were counted by histological examination.
  • Results showed that a significant enhancement of proliferative and cytotoxic activities accompanied with increased IFN-gamma and TNF-alpha production as well as decreased IL-4 production were obtained from the mice vaccinated with 4T1-ITAC.
  • The number of clonogenic metastatic tumor cells in the mice vaccinated with 4T1-ITAC cells reduced markedly and no visible metastasis was found in the lungs of the 4T1-ITAC vaccinated mice.
  • Taken together, our results demonstrated that ITAC-modified tumor cell vaccine can enhance the anti-tumor immunity and reduce the incidence of disseminated metastasis.
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL11. Colon / pathology. Cytokines / biosynthesis. Cytotoxicity Tests, Immunologic. Female. Histocytochemistry. Lung / pathology. Mice. Mice, Inbred BALB C. T-Lymphocytes / immunology. Vaccines, Synthetic / genetics. Vaccines, Synthetic / immunology

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  • (PMID = 16503368.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Chemokine CXCL11; 0 / Chemokines, CXC; 0 / Cxcl11 protein, mouse; 0 / Cytokines; 0 / Vaccines, Synthetic
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15. Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C: Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells). Adv Exp Med Biol; 2008;606:217-40
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  • [Title] Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells).
  • HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a molecular complex derived from human milk that kills tumor cells by a process resembling programmed cell death.
  • The complex consists of partially unfolded alpha-lactalbumin and oleic acid, and both the protein and the fatty acid are required for cell death.
  • The mechanisms of tumor cell death remain unclear, however.
  • Immediately after the encounter with tumor cells, HAMLET invades the cells and causes mitochondrial membrane depolarization, cytochrome c release, phosphatidyl serine exposure, and a low caspase response.
  • A fraction of the cells undergoes morphological changes characteristic of apoptosis, but caspase inhibition does not rescue the cells and Bcl-2 overexpression or altered p53 status does not influence the sensitivity of tumor cells to HAMLET.
  • HAMLET also creates a state of unfolded protein overload and activates 20S proteasomes, which contributes to cell death.
  • In parallel, HAMLET translocates to tumor cell nuclei, where high-affinity interactions with histones cause chromatin disruption, loss of transcription, and nuclear condensation.
  • The dying cells also show morphological changes compatible with macroautophagy, and recent studies indicate that macroautophagy is involved in the cell death response to HAMLET.
  • The results suggest that HAMLET, like a hydra with many heads, may interact with several crucial cellular organelles, thereby activating several forms of cell death, in parallel.
  • This complexity might underlie the rapid death response of tumor cells and the broad antitumor activity of HAMLET.

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  • (PMID = 18183931.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HAMLET complex, human; 0 / Oleic Acids; 9013-90-5 / Lactalbumin
  • [Number-of-references] 122
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16. LaMarca B, Speed J, Fournier L, Babcock SA, Berry H, Cockrell K, Granger JP: Hypertension in response to chronic reductions in uterine perfusion in pregnant rats: effect of tumor necrosis factor-alpha blockade. Hypertension; 2008 Dec;52(6):1161-7
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  • [Title] Hypertension in response to chronic reductions in uterine perfusion in pregnant rats: effect of tumor necrosis factor-alpha blockade.
  • Reductions in uterine perfusion pressure (RUPP) in pregnant rats is associated with increased tumor necrosis factor-alpha (TNF-alpha).
  • This study was designed to determine the role of endogenous TNF-alpha in mediating changes in arterial pressure and endothelin-1 (ET-1) in RUPP rats.
  • To achieve this goal we examined the effect of RUPP in the presence and absence of a TNF-alpha-soluble receptor, etanerecept (0.4 mg/kg).
  • Serum TNF-alpha increased to 40+/-7.6 pg/mL in RUPP rats (n=24) versus 14.8+/-3.3 pg/mL (n=16; P<0.05) in NP rats.
  • Administration of etanerecept decreased TNF-alpha in RUPP rats (n=20) to 17.2+/-3 pg/mL and mean arterial pressure to 118+/-2 mm Hg (P<0.05).
  • The direct effect of TNF-alpha blockade on endothelial activation in response to placental ischemia was examined in human umbilical vein endothelial cells.
  • ET-1 secreted from human umbilical vein endothelial cells treated with RUPP serum was 59.2+16 pg/mg and decreased when etanerecept was added to the medium with RUPP serum (7.60+/-0.77 pg/mg), as well as in response to serum from etanerecept-treated RUPP rats (7.30+/-0.55 pg/mg; P<0.001).
  • ET-1 secreted from human umbilical vein endothelial cells was 15.6+/-2 pg/mg when treated with NP serum.
  • These data support the hypothesis that endogenous TNF-alpha is an important stimulus for ET-1 in response to placental ischemia and is important in mediating endothelial cell activation and hypertension during pregnancy.

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  • (PMID = 18981324.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL78147; United States / NHLBI NIH HHS / HL / P01 HL051971; United States / NHLBI NIH HHS / HL / F32 HL078147; United States / NHLBI NIH HHS / HL / P01 HL051971-150002; United States / NHLBI NIH HHS / HL / HL051971-150002; United States / NHLBI NIH HHS / HL / HL051971; United States / NHLBI NIH HHS / HL / F32 HL078147-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / Immunoglobulin G; 0 / Immunologic Factors; 0 / RNA, Messenger; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  • [Other-IDs] NLM/ NIHMS159091; NLM/ PMC2788766
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17. Li H, Li X, Gao X, Lu X: [Induction of apoptosis by tumor necrosis factor receptors 2 transgene in human laryngeal squamous cacinoma in nude mice animal model]. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi; 2009 Feb;23(3):125-9
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  • [Title] [Induction of apoptosis by tumor necrosis factor receptors 2 transgene in human laryngeal squamous cacinoma in nude mice animal model].
  • OBJECTIVE: To investigate the effect of tumor necrosis factor receptors II (TNFR II) in vivo transgene with topical injection of TNF alpha in inducing apoptosis and cell killing of laryngeal squamous carcinoma in nude mice animal model.
  • TNF alpha was topically injected into tumor.
  • Goss measurement of tumor, flow cytometry, immunohistochemistry, tunel and transmission electron microscopy were conducted to observe the expression of TNFR II protein and the apoptosis of tumor cells, and the effects of tumor killing and growth inhibition was objectively evaluated.
  • Immunohistochemistry showed the expression of TNFR II is mainly on the cell membrane of the transfected tumor cells.
  • Topical injection of 2000 U TNF alpha was most efficient in inducing tumor cell apoptosis, cell inhibition and cell killing.
  • The tumor volume, weight, and tumor/body ratio in TNFR II transfected group were (1161.333 +/- 166.555) mm3, (1.100 +/- 0.832) g and 0.044 +/- 0.332, respectively, with a corresponding high level of tumor cell apoptosis rate (38.226 +/- 13.671) %, all of which were significantly higher than that in non-transfected group.
  • Tunel and ultrastructural observations demonstrated apoptosis-related changes in the transfected tumor cells.
  • CONCLUSION: Up-regulation of TNFR II expression by in vivo gene transfection on tumor cells can remarkably enhance the tumor cell killing effect of topical injection of TNF-alpha.
  • In vivo transgene of TNFR II in combination with topical injection of TNF alpha may become a effective gene therapy method in treating laryngeal cancer.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Squamous Cell / pathology. Laryngeal Neoplasms / pathology. Receptors, Tumor Necrosis Factor, Type II / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Genetic Therapy / methods. Humans. Mice. Mice, Nude. Transfection. Transgenes. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 19452731.001).
  • [ISSN] 1001-1781
  • [Journal-full-title] Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery
  • [ISO-abbreviation] Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
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18. Tse AK, Wan CK, Shen XL, Yang M, Fong WF: Honokiol inhibits TNF-alpha-stimulated NF-kappaB activation and NF-kappaB-regulated gene expression through suppression of IKK activation. Biochem Pharmacol; 2005 Nov 15;70(10):1443-57
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  • [Title] Honokiol inhibits TNF-alpha-stimulated NF-kappaB activation and NF-kappaB-regulated gene expression through suppression of IKK activation.
  • In this study, we investigated whether honokiol affects the transcription factor nuclear factor-kappa B (NF-kappaB) which controls a large number of genes involved in angiogenesis, metastasis and cell survival.
  • We observed that the tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB activation was blocked by honokiol in four different cancer cell lines as evidenced by EMSA.
  • Immunoblot experiments demonstrated that honokiol inhibited the TNF-alpha-stimulated phosphorylation and degradation of the cytosolic NF-kappaB inhibitor IkappaBalpha.
  • Furthermore, honokiol suppressed the intrinsic and TNF-alpha-stimulated upstream IkappaB kinases (IKKs) activities measured by a non-radioactive kinase assay using immunoprecipitated IKKs, suggesting a critical role of honokiol in abrogating the phosphorylation and degradation of IkappaBalpha.
  • In a HeLa cell NF-kappaB-dependent luciferase reporter system, honokiol suppressed luciferase expression stimulated by TNF-alpha and by the transient transfection and expression of NIK (NF-kappaB-inducing kinase), wild type IKKbeta, constitutively active IKKalpha and IKKbeta, or the p65 subunit.
  • RT-PCR results showed that honokiol suppressed NF-kappaB-regulated inflammatory and carcinogenic gene products including MMP-9, TNF-alpha, IL-8, ICAM-1 and MCP-1.
  • In line with the observation that NF-kappaB activation may up-regulate anti-apoptotic genes, it was shown that honokiol enhanced TNF-alpha-induced apoptotic cell death.
  • In summary, our results demonstrate that honokiol suppresses NF-kappaB activation and NF-kappaB-regulated gene expression through the inhibition of IKKs, which provides a possible mechanism for its anti-tumor actions.
  • [MeSH-major] Biphenyl Compounds / pharmacology. I-kappa B Kinase / metabolism. Lignans / pharmacology. NF-kappa B / antagonists & inhibitors. NF-kappa B / genetics. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Electrophoretic Mobility Shift Assay / methods. Gene Expression / drug effects. Genes, Reporter / physiology. Humans. Lipopolysaccharides / antagonists & inhibitors. Lipopolysaccharides / pharmacology. Luciferases / antagonists & inhibitors. Luciferases / drug effects. Luciferases / genetics. Lymphotoxin-alpha / metabolism. NF-kappa B p50 Subunit / drug effects. NF-kappa B p50 Subunit / metabolism. Phosphorylation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tetradecanoylphorbol Acetate / antagonists & inhibitors. Tetradecanoylphorbol Acetate / pharmacology. Transcription Factor AP-1 / antagonists & inhibitors. Transcription Factor AP-1 / drug effects. Transcription Factor RelA / drug effects. Transcription Factor RelA / metabolism

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  • (PMID = 16181613.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Lignans; 0 / Lipopolysaccharides; 0 / Lymphotoxin-alpha; 0 / NF-kappa B; 0 / NF-kappa B p50 Subunit; 0 / Transcription Factor AP-1; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 11513CCO0N / honokiol; EC 1.13.12.- / Luciferases; EC 2.7.11.10 / I-kappa B Kinase; NI40JAQ945 / Tetradecanoylphorbol Acetate
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19. Neuzil J, Dong LF, Wang XF, Zingg JM: Tocopherol-associated protein-1 accelerates apoptosis induced by alpha-tocopheryl succinate in mesothelioma cells. Biochem Biophys Res Commun; 2006 May 19;343(4):1113-7
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  • [Title] Tocopherol-associated protein-1 accelerates apoptosis induced by alpha-tocopheryl succinate in mesothelioma cells.
  • Alpha-tocopheryl succinate (alpha-TOS), a redox-silent analogue of vitamin E, induces apoptosis in multiple cell lines in a selective manner, by activating the intrinsic pathway.
  • We studied the role of the ubiquitous tocopherol-associated protein-1 (TAP1 or sec14-like 2) in apoptosis induction by alpha-TOS in malignant mesothelioma (MM) cells.
  • Over-expression of TAP1 in MM cells sensitised them to apoptosis by low doses of alpha-TOS which were sub-apoptotic for the parental cells.
  • Apoptosis induced in TAP1-over-expressing cells was mitochondria- and caspase-dependent, as suggested by dissipation of mitochondrial trans-membrane potential and inhibition by zVAD-fmk, respectively.
  • Binding assays showed affinity of alpha-TOS for TAP1.
  • Finally, TAP1 over-expressing cells accumulated alpha-TOS at higher levels compared to their normal counterparts.
  • We suggest that TAP1 may act as an intracellular shuttle for alpha-TOS, promoting apoptosis initiated by this vitamin E analogue, as shown here for MM cells.
  • [MeSH-minor] Caspases / metabolism. Cell Line, Tumor. Humans. Membrane Potentials. Mitochondria / physiology. Tocopherols

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  • (PMID = 16579965.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Lipoproteins; 0 / SEC14L2 protein, human; 0 / Trans-Activators; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols; EC 3.4.22.- / Caspases
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20. Cuesta A, Angeles Esteban M, Meseguer J: Cloning, distribution and up-regulation of the teleost fish MHC class II alpha suggests a role for granulocytes as antigen-presenting cells. Mol Immunol; 2006 Mar;43(8):1275-85
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  • [Title] Cloning, distribution and up-regulation of the teleost fish MHC class II alpha suggests a role for granulocytes as antigen-presenting cells.
  • The major histocompatibility complex (MHC) class II alpha chain gene of the teleost fish gilthead seabream (Sparus aurata), Spau-DAA, has been characterized.
  • We cloned, sequenced and studied its polymorphism, before evaluating its expression in resting seabream leucocytes, tissues and tumor cells as well as in primed leucocytes.
  • The putative protein of 242 residues shows homology with known MHC class II alpha genes, varying from 71 to 28% in other fish and humans, respectively.
  • The protein sequence showed all the important features: leader peptide, alpha1, alpha2 and CP/TM/CYT regions, conserved cysteines and N-glycosylation site.
  • Apart from these granulocytes lymphocytes also express the Spau-DAA gene, although other cell types may also do the same.
  • Finally, incubation of head-kidney leucocytes with yeast cells or pathogenic bacteria up-regulates Spau-DAA gene expression whilst incubation with ConA, ConA+LPS or PHA does not.
  • The possible involvement of the seabream MHC class II alpha gene in the fish defence and antigen presentation are discussed.
  • [MeSH-major] Antigen-Presenting Cells / immunology. Genes, MHC Class II / genetics. Granulocytes / immunology. Granulocytes / metabolism. Histocompatibility Antigens Class II / genetics. Sea Bream / genetics. Up-Regulation / genetics

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  • (PMID = 16168483.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ019401
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II; 0 / RNA, Messenger
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21. Ye Z, Chen Z, Sami A, El-Gayed A, Xiang J: Human dendritic cells engineered to express alpha tumor necrosis factor maintain cellular maturation and T-cell stimulation capacity. Cancer Biother Radiopharm; 2006 Dec;21(6):613-22
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  • [Title] Human dendritic cells engineered to express alpha tumor necrosis factor maintain cellular maturation and T-cell stimulation capacity.
  • Dendritic cell (DC) vaccine has been demonstrated to induce antitumor immunity in animal models.
  • The mature human DCs generated from peripheral blood mononuclear cells (PBMCs) in the presence of granulocyte macrophage-colony-stimulating factor (GM-CSF), interleukin (IL)-4, and tumor necrosis factor (TNF)-alpha have widely contributed to their growing use in cancer vaccination trials.
  • In this study, we investigated the influence of different culture media (RPMI 1640/10% fetal calf serum [FCS] versus serum-free AIM-V medium) on DC maturation and the change of maturation status of these ex vivo generated mature DCs during further culturing in medium without inflammatory cytokine TNF-alpha.
  • We previously constructed a recombinant adenovirus AdV-TNF-alpha expressing the transgene human TNF-alpha.
  • We transfected human DCs with AdV-TNF-alpha at multiplicity of infection of 100, resulting in engineered DCs secreting TNF-alpha (4.6 ng/mL/10(6) cells/24 hours).
  • We also conducted kinetic studies to compare the maturation status and the T-cell stimulation capacity by ex vivo-generated mature DCs and TNF-alpha- transgene-engineered DCs during further culturing in medium without TNF-alpha.
  • Our data show that mature DCs can be generated from PBMCs in both Dulbecco's modified Eagle's medium plus 10% FCS and serum-free AIM-V medium containing GM-CSF (100 ng/mL), IL-4 (100 ng/mL), and TNF-alpha (10 ng/mL).
  • However, these mature DCs gradually lost their maturity and became immature ones when culturing in medium in the absence of TNF-alpha.
  • On the contrary, the human DCs engineered to express TNF-alpha can (i) stably maintain their cellular maturation and (ii) efficiently stimulate T-cell proliferation even during culturing ex vivo in medium without TNF-alpha stimulation.
  • Therefore, DCs engineered to express TNF-alpha may also maintain their maturation status and induce more efficient antitumor immune responses when applied in vivo for vaccination.
  • [MeSH-major] Cell Differentiation. Dendritic Cells / cytology. Dendritic Cells / metabolism. Gene Expression. T-Lymphocytes / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Cells, Cultured. Culture Media, Serum-Free. Humans. Lymphocyte Activation. Lymphocyte Culture Test, Mixed. Phenotype. Protein Engineering. Receptors, CCR7. Receptors, Chemokine / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Recombinant Proteins / pharmacology

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  • (PMID = 17257077.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR7 protein, human; 0 / Culture Media, Serum-Free; 0 / Receptors, CCR7; 0 / Receptors, Chemokine; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
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22. Shvero J, Koren R, Shvili I, Yaniv E, Sadov R, Hadar T: Expression of human DNA Topoisomerase II-alpha in squamous cell carcinoma of the larynx and its correlation with clinicopathologic variables. Am J Clin Pathol; 2008 Dec;130(6):934-9
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  • [Title] Expression of human DNA Topoisomerase II-alpha in squamous cell carcinoma of the larynx and its correlation with clinicopathologic variables.
  • The aggressiveness of laryngeal squamous cell carcinoma (SCC) is unpredictable.
  • Topoisomerase (Topo) II-alpha is an essential nuclear enzyme; its expression rises at the end of the S-G2/M phase and drops at completion of mitosis.
  • This study sought to determine if Topo II-alpha expression can serve as a prognostic factor in laryngeal SCC.
  • Specimens from 56 consecutive patients were immunohistochemically stained for Topo II-alpha, and the number of positive cells in the areas of highest staining was counted in 3 highpower fields (X400) (Topo II-alpha index).
  • Differences in the Topo II-alpha index by the presence or absence of recurrence, tumor stage and grade, and disease course were analyzed statistically.
  • On multivariate Cox regression analysis, the Topo II-alpha index (>70 or < or =70) (P = .008) and tumor grade (P = .034) independently predicted disease-free survival.
  • These findings suggest that high Topo II-alpha expression may be a useful indicator of tumor aggressiveness and poor outcome in laryngeal SCC.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Biomarkers, Tumor / biosynthesis. DNA Topoisomerases, Type II / biosynthesis. DNA-Binding Proteins / biosynthesis. Laryngeal Neoplasms / metabolism. Neoplasms, Squamous Cell / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 19019771.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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23. Wada Y, Yoshida K, Hihara J, Konishi K, Tanabe K, Ukon K, Taomoto J, Suzuki T, Mizuiri H: Sivelestat, a specific neutrophil elastase inhibitor, suppresses the growth of gastric carcinoma cells by preventing the release of transforming growth factor-alpha. Cancer Sci; 2006 Oct;97(10):1037-43
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  • [Title] Sivelestat, a specific neutrophil elastase inhibitor, suppresses the growth of gastric carcinoma cells by preventing the release of transforming growth factor-alpha.
  • In the present study, we investigated whether NE promotes cell growth by activation of EGFR to elucidate whether surgical stress induces tumor proliferation and progression.
  • Furthermore, we examined the antitumor effect of a specific NE inhibitor, sivelestat.
  • Cell growth assays were carried out in vitro and in vivo using TMK-1 gastric cancer cells.
  • TMK-1 cell growth was stimulated to 118% of that of the control cells after 48 h stimulation with 1 microg/mL NE according to an MTT assay.
  • Sivelestat inhibited cell growth to 23.4 and 58.0% of control values at concentrations of 100 and 1,000 microg/mL, respectively.
  • It was further demonstrated that NE-induced EGFR phosphorylation was transactivated through TGF-alpha, using ELISA.
  • NE increased the cleavage of TGF-alpha from the cell surface 30-fold compared with the cells without treatment.
  • Interestingly, sivelestat significantly reduced NE-induced EGFR phosphorylation and ERK1/2 activation and completely blocked the release of TGF-alpha from the TMK-1 cell surface.
  • In a xenograft study, the addition of ventrotomy as a surgical stress promoted tumor growth.
  • Sivelestat significantly suppressed the tumor growth induced by surgical stress.
  • These results indicate that sivelestat suppresses the growth of gastric cancer cells by inhibiting the release of TGF-alpha stimulated by NE, which often occurs after surgical stresses.
  • [MeSH-major] Carcinoma / drug therapy. Glycine / analogs & derivatives. Leukocyte Elastase / antagonists & inhibitors. Serine Proteinase Inhibitors / therapeutic use. Stomach Neoplasms / drug therapy. Sulfonamides / therapeutic use. Transforming Growth Factor alpha / antagonists & inhibitors

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  • (PMID = 16918998.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Serine Proteinase Inhibitors; 0 / Sulfonamides; 0 / Transforming Growth Factor alpha; DWI62G0P59 / sivelestat; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.37 / Leukocyte Elastase; TE7660XO1C / Glycine
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24. Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH: Alpha-fetoprotein-producing pancreatic acinar cell carcinoma. J Formos Med Assoc; 2007 Aug;106(8):669-72
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  • [Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
  • A 47-year-old man with chronic hepatitis B had progressive elevated alpha-fetoprotein of 2 years' duration.
  • A pancreatic tail tumor, instead of liver tumor, was detected.
  • He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.
  • Serum level of alpha-fetoprotein returned to normal soon after surgery.
  • Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.
  • However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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  • (PMID = 17711801.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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25. Kang JH, Oishi J, Kim JH, Ijuin M, Toita R, Jun B, Asai D, Mori T, Niidome T, Tanizawa K, Kuroda S, Katayama Y: Hepatoma-targeted gene delivery using a tumor cell-specific gene regulation system combined with a human liver cell-specific bionanocapsule. Nanomedicine; 2010 Aug;6(4):583-9
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  • [Title] Hepatoma-targeted gene delivery using a tumor cell-specific gene regulation system combined with a human liver cell-specific bionanocapsule.
  • Hepatoma (hepatocellular carcinoma) is the most common type of malignant tumor originating in the liver and has a relatively low 5-year survival rate.
  • The gene delivery system was prepared by combining a human liver cell-specific bionanocapsule (BNC) and a tumor cell-specific gene regulation polymer, which responds to hyperactivated protein kinase C alpha in hepatoma cells.
  • The complex of the polymer-DNA with BNCs was delivered into cells and tissues.
  • The developed system showed increased transfection efficiency and resulted in cell-specific gene expression in hepatoma cells and tissues (HuH-7), but no gene expression in normal human hepatocytes or human epidermoid tumor cells (A431).
  • The combination of a tumor cell-specific gene regulation system responding to protein kinase C alpha and BNCs showed excellent potential for the selective treatment of hepatomas.
  • From the clinical editor: Hepatocellular carcinoma is the most common type of malignant tumor in the liver with a low 5-year survival rate.
  • In this study, a novel hepatoma-targeted gene delivery system was prepared by combining a human liver cell-specific bionanocapsule and a tumor cell-specific gene regulation polymer, which responds to hyperactivated protein kinase C (PKC)a in hepatoma cells.
  • [MeSH-minor] Animals. Gene Expression Regulation. Gene Transfer Techniques. Hepatocytes / metabolism. Hepatocytes / pathology. Humans. Liver / pathology. Male. Mice. Oligopeptides / chemistry. Tumor Cells, Cultured

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Nanomedicine. 2011 Aug;7(4):514
  • (PMID = 20138242.001).
  • [ISSN] 1549-9642
  • [Journal-full-title] Nanomedicine : nanotechnology, biology, and medicine
  • [ISO-abbreviation] Nanomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nanocapsules; 0 / Oligopeptides
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26. Romagnoli R, Baraldi PG, Cruz-Lopez O, Lopez-Cara C, Preti D: alpha-halogenoacrylic derivatives of antitumor agents. Mini Rev Med Chem; 2009 Jan;9(1):81-94
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  • [Title] alpha-halogenoacrylic derivatives of antitumor agents.
  • In this review article we have reported a series of hybrid compounds characterized by the presence of a alpha-halogenocryloyl alkylating moiety of low chemical reactivity, linked to known antitumor agents or their active moieties.
  • [MeSH-minor] Animals. Cell Line, Tumor. Distamycins / chemistry. Distamycins / pharmacology. Guanidines / chemistry. Guanidines / therapeutic use. Humans. Mice. Pyrroles / chemistry. Pyrroles / therapeutic use

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  • (PMID = 19149662.001).
  • [ISSN] 1389-5575
  • [Journal-full-title] Mini reviews in medicinal chemistry
  • [ISO-abbreviation] Mini Rev Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Distamycins; 0 / Guanidines; 0 / Pyrroles; 0 / Pyrroloiminoquinones; 80O63P88IS / stallimycin; RPC6R41K4I / brostallicin
  • [Number-of-references] 43
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27. Ayalasomayajula SP, Ashton P, Kompella UB: Fluocinolone inhibits VEGF expression via glucocorticoid receptor in human retinal pigment epithelial (ARPE-19) cells and TNF-alpha-induced angiogenesis in chick chorioallantoic membrane (CAM). J Ocul Pharmacol Ther; 2009 Apr;25(2):97-103
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  • [Title] Fluocinolone inhibits VEGF expression via glucocorticoid receptor in human retinal pigment epithelial (ARPE-19) cells and TNF-alpha-induced angiogenesis in chick chorioallantoic membrane (CAM).
  • PURPOSE: The purpose of this study was to determine whether fluocinolone inhibits vascular endothelial growth factor (VEGF) expression in a retinal pigment epithelial cell line (ARPE-19) and TNF-alpha-induced angiogenesis in chick chorioallantoic membrane (CAM) assay.
  • METHODS: The dose-dependent effect of fluocinolone (0.0001-1 microM) on VEGF secretion, VEGF mRNA expression, and cytotoxicity was determined in confluent monolayers of ARPE-19 cells using ELISA, RT-PCR, and MTT assay, respectively.
  • The effect of a glucocorticoid receptor antagonist (RU486) on fluocinolone-mediated VEGF expression was determined.
  • The effect of fluocinolone in inhibiting TNF-alpha-induced angiogenesis was determined using chick chorioallantoic membrane (CAM) assay.
  • The dose-dependent effect of fluocinolone (0.0001-1 microM) in inhibiting 1% serum-stimulated ARPE-19 cell proliferation was determined using BrdU labeling assay.
  • RESULTS: At concentrations devoid of cytotoxicity, fluocinolone inhibited VEGF secretion as well as mRNA expression in ARPE-19 cells.
  • Fluocinolone (50 ng/egg) inhibited angiogenesis induced by TNF-alpha.
  • The ARPE-19 cell proliferation was inhibited by fluocinolone in a dose-dependent manner.
  • CONCLUSIONS: Fluocinolone inhibited VEGF expression in ARPE-19 cells via its glucocorticoid receptor activity.
  • In addition, fluocinolone inhibited proliferation of ARPE-19 cells and TNF-alpha-induced angiogenesis in chorioallantoic membranes.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Chorioallantoic Membrane / drug effects. Fluocinolone Acetonide / analogs & derivatives. Receptors, Glucocorticoid / metabolism. Retinal Pigment Epithelium / drug effects. Tumor Necrosis Factor-alpha / metabolism. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line. Cell Proliferation / drug effects. Chick Embryo. Enzyme-Linked Immunosorbent Assay. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Humans. Mifepristone / metabolism. Mifepristone / pharmacology. Neovascularization, Physiologic / drug effects. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19284324.001).
  • [ISSN] 1557-7732
  • [Journal-full-title] Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
  • [ISO-abbreviation] J Ocul Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / RNA, Messenger; 0 / Receptors, Glucocorticoid; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 0CD5FD6S2M / Fluocinolone Acetonide; 320T6RNW1F / Mifepristone; CT1IX58L9S / fluocinolone
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28. Papageorgiou A, Kamat A, Benedict WF, Dinney C, McConkey DJ: Combination therapy with IFN-alpha plus bortezomib induces apoptosis and inhibits angiogenesis in human bladder cancer cells. Mol Cancer Ther; 2006 Dec;5(12):3032-41
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  • [Title] Combination therapy with IFN-alpha plus bortezomib induces apoptosis and inhibits angiogenesis in human bladder cancer cells.
  • In a recent study, we showed that the proteasome inhibitor bortezomib sensitizes human bladder cancer cells to IFN-induced cell death.
  • Bortezomib synergized with IFN-alpha to promote apoptosis via a tumor necrosis factor-related apoptosis-inducing ligand-associated mechanism but did not inhibit production of proangiogenic factors (vascular endothelial growth factor, basic fibroblast growth factor, and interleukin-8) in human UM-UC-5 cells.
  • In contrast, exposure to the combination did not increase the levels of apoptosis in human UM-UC-3 cells but did inhibit the production of basic fibroblast growth factor and vascular endothelial growth factor.
  • Studies with tumor xenografts confirmed that combination therapy with bortezomib plus IFN-alpha was effective in both models but that the effects were associated with differential effects on tumor necrosis factor-related apoptosis-inducing ligand-associated apoptosis (predominant in UM-UC-5) versus inhibition of angiogenesis (predominant in UM-UC-3).
  • Together, our results show that combination therapy with IFN-alpha plus bortezomib is effective but can work via different mechanisms (apoptosis versus angiogenesis inhibition) in preclinical models of human bladder cancer.
  • [MeSH-minor] Animals. Boronic Acids / administration & dosage. Bortezomib. Cell Growth Processes / drug effects. Fibroblast Growth Factor 2 / biosynthesis. Humans. Interferon-alpha / administration & dosage. Interleukin-8 / biosynthesis. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Pyrazines / administration & dosage. TNF-Related Apoptosis-Inducing Ligand / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis. Xenograft Model Antitumor Assays

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  • [ErratumIn] Mol Cancer Ther. 2009 Feb;8(2):480
  • (PMID = 17172406.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA91846
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Interferon-alpha; 0 / Interleukin-8; 0 / Pyrazines; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 69G8BD63PP / Bortezomib
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29. Yang S, Lin L, Chen JX, Lee CR, Seubert JM, Wang Y, Wang H, Chao ZR, Tao DD, Gong JP, Lu ZY, Wang DW, Zeldin DC: Cytochrome P-450 epoxygenases protect endothelial cells from apoptosis induced by tumor necrosis factor-alpha via MAPK and PI3K/Akt signaling pathways. Am J Physiol Heart Circ Physiol; 2007 Jul;293(1):H142-51
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  • [Title] Cytochrome P-450 epoxygenases protect endothelial cells from apoptosis induced by tumor necrosis factor-alpha via MAPK and PI3K/Akt signaling pathways.
  • Endothelial cells play a vital role in the maintenance of cardiovascular homeostasis.
  • Epoxyeicosatrienoic acids (EETs), cytochrome P-450 (CYP) epoxygenase metabolites of arachidonic acid in endothelial cells, possess potent and diverse biological effects within the vasculature.
  • We evaluated the effects of overexpression of CYP epoxygenases on tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis in bovine aortic endothelial cells.
  • CYP epoxygenase overexpression significantly increased endothelial cell viability and inhibited TNF-alpha induction of endothelial cell apoptosis as evaluated by morphological analysis of nuclear condensation, DNA laddering, and fluorescent-activated cell sorting (FACS) analysis.
  • CYP epoxygenase overexpression also significantly inhibited caspase-3 activity and downregulation of Bcl-2 expression induced by TNF-alpha.
  • Furthermore, CYP epoxygenase overexpression significantly attenuated the extent of TNF-alpha-induced ERK1/2 dephosphorylation in a time-dependent manner and significantly increased PI3K expression and Akt phosphorylation in both the presence and absence of TNF-alpha.
  • Collectively, these results suggest that CYP epoxygenase overexpression, which is known to increase EET biosynthesis, significantly protects endothelial cells from apoptosis induced by TNF-alpha.
  • [MeSH-major] Cytochrome P-450 Enzyme System / metabolism. Endothelial Cells / metabolism. MAP Kinase Signaling System / physiology. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Apoptosis / physiology. Cattle. Cells, Cultured

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  • (PMID = 17322420.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES025034-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS33442; NLM/ PMC2100428
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30. Tangpong J, Cole MP, Sultana R, Joshi G, Estus S, Vore M, St Clair W, Ratanachaiyavong S, St Clair DK, Butterfield DA: Adriamycin-induced, TNF-alpha-mediated central nervous system toxicity. Neurobiol Dis; 2006 Jul;23(1):127-39
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  • [Title] Adriamycin-induced, TNF-alpha-mediated central nervous system toxicity.
  • The present study demonstrates that ADR autofluorescence was detected only in areas of the brain located outside the blood-brain barrier, but a strong tumor necrosis factor (TNF) alpha immunoreactivity was detected in the cortex and hippocampus of ADR-treated mice.
  • Cytochrome c release, increased caspase 3 activity, and TUNEL-positive cell death all were suggestive of apoptosis in brain following systemic ADR treatment.
  • [MeSH-major] Antibiotics, Antineoplastic / toxicity. Brain / drug effects. Doxorubicin / toxicity. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3. Caspases / drug effects. Caspases / metabolism. Cell Respiration / drug effects. Cytochromes c / drug effects. Cytochromes c / metabolism. Enzyme-Linked Immunosorbent Assay. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mitochondria / drug effects. Mitochondria / metabolism. Mitochondria / pathology. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein / drug effects. bcl-2-Associated X Protein / metabolism. bcl-X Protein / drug effects. bcl-X Protein / metabolism

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  • (PMID = 16697651.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG-05119; United States / NIA NIH HHS / AG / AG-10836; United States / NCI NIH HHS / CA / CA-80152; United States / NCI NIH HHS / CA / CA-94853
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Bcl2l1 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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31. Ohmura Y, Yoshikawa K, Saga S, Ueda R, Kazaoka Y, Yamada S: Combinations of tumor-specific CD8+ CTLs and anti-CD25 mAb provide improved immunotherapy. Oncol Rep; 2008 May;19(5):1265-70
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  • [Title] Combinations of tumor-specific CD8+ CTLs and anti-CD25 mAb provide improved immunotherapy.
  • One new approach to cancer therapy is based on the adoptive transfer of tumor-specific cytotoxic T cells and anti-CD25 antibodies.
  • In the present study, CD8+ and IFN-gamma secreting T lymphocytes (CTLs) were enriched as tumor-specific cytotoxic T cells from spleen lymphocytes of mice bearing the Renca tumor (a murine renal carcinoma line originating from a BALB/c mouse) after stimulation with tumor cells.
  • An anti-CD25 IL-2Ralpha(anti-CD25) mAb from hybridoma PC61 was used for depletion for CD4(+)CD25(+) regulatory T (Treg) cells.
  • Treatment-efficacy for tumor-bearing mice was compared using 4 systems: 1, whole spleen lymphocytes stimulated with tumor cells in vitro from tumor-bearing mice; 2, CTLs; 3, anti-CD25 mAbs; 4, CTLs and anti-CD25 mAbs.
  • At the 50th day after tumor inoculation, in the group which received anti-CD25 mAb for depletion of T cells and inoculation of CTLs, tumors had disappeared and no re-growth was observed.
  • In contrast, all mice of the non-treated and other three groups, treated with whole spleen cells alone, CTLs alone and anti-CD25 mAb alone, had died.
  • These results showed that a combination of Treg cell-depletion using anti-CD25 mAbs and CTL administration is a feasible approach for treatment of cancers which warrants further exploration in the clinical setting.
  • [MeSH-major] Antibodies, Monoclonal / chemistry. CD8-Positive T-Lymphocytes / pathology. Interleukin-2 Receptor alpha Subunit / biosynthesis. T-Lymphocytes, Cytotoxic / metabolism. T-Lymphocytes, Regulatory / cytology
  • [MeSH-minor] Animals. Cell Line, Tumor. Chromium Isotopes / chemistry. Female. Immunotherapy, Adoptive / methods. Interferon-gamma / metabolism. Medical Oncology / methods. Mice. Mice, Inbred BALB C. Models, Biological

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  • (PMID = 18425386.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Chromium Isotopes; 0 / Interleukin-2 Receptor alpha Subunit; 82115-62-6 / Interferon-gamma
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32. Cagli KE, Aras D, Topaloglu S, Geyik B, Ayaz S, Cagirci G, Kisacik HL, Korkmaz S: Plasma levels of tumor necrosis factor-alpha and its receptors in patients with mitral stenosis and sinus rhythm undergoing percutaneous balloon valvuloplasty. Heart Vessels; 2010 Mar;25(2):131-7
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  • [Title] Plasma levels of tumor necrosis factor-alpha and its receptors in patients with mitral stenosis and sinus rhythm undergoing percutaneous balloon valvuloplasty.
  • This study aimed to determine whether plasma levels of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptor (sTNF-R) increases in rheumatic mitral stenosis (MS) patients with sinus rhythm and to examine the effect of percutaneous mitral balloon valvuloplasty (PMBV) on these parameters.
  • Tumor necrosis factor-alpha and sTNF-R levels were compared between study patients and controls, and between peripheral and left atrium (LA) blood.
  • Changes in TNF alpha and sTNF-R levels 24 h and 4 weeks after PMBV were analyzed.
  • Significantly higher baseline TNF-alpha and sTNF-R levels were noted in the study group.
  • In the study group, TNF-alpha and its receptors were also found to be higher in LA blood than in baseline peripheral blood.
  • At the 24th hour after PMBV, the TNF-alpha level decreased from 29.61 +/- 12.22 pg/ml to 22.42 +/- 8.81 pg/ml (P < 0.0001) and at the 4th week, from 22.42 +/- 8.81 pg/ml to 18.92 +/- 7.37 pg/ml (P < 0.0001).
  • This study suggests that isolated rheumatic MS without atrial fibrillation is accompanied by increased TNF-alpha and sTNF-R level.
  • The successful PMBV establishes a significant reduction in TNF-alpha and its receptors, probably due to improved postprocedural hemodynamic parameters.
  • [MeSH-major] Catheterization. Heart Conduction System / physiopathology. Inflammation Mediators / blood. Mitral Valve Stenosis / therapy. Receptors, Tumor Necrosis Factor / blood. Rheumatic Heart Disease / therapy. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 20339974.001).
  • [ISSN] 1615-2573
  • [Journal-full-title] Heart and vessels
  • [ISO-abbreviation] Heart Vessels
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Inflammation Mediators; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha
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33. Cao B, Chen XP, Zhu P, Ding L, Guan J, Shi ZL: Inhibitory effect of interferon-alpha-2b on expression of cyclooxygenase-2 and vascular endothelial growth factor in human hepatocellular carcinoma inoculated in nude mice. World J Gastroenterol; 2008 Nov 28;14(44):6802-7
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  • [Title] Inhibitory effect of interferon-alpha-2b on expression of cyclooxygenase-2 and vascular endothelial growth factor in human hepatocellular carcinoma inoculated in nude mice.
  • AIM: To evaluate the effects of interferon-alpha-2b (IFN-alpha-2b) on expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in human hepatocellular carcinoma (HCC) inoculated in nude mice and to study the underlying mechanism of IFN-alpha-2b against HCC growth.
  • On the 10th day after implantation of HCC cells, the mice in test groups (groups A, B and C) received IFN-alpha-2b at a serial dose (10000 IU for group A, 20000 IU for group B, 40000 IU for group C sc daily) for 35 d.
  • The growth conditions of transplanted tumors were observed.
  • Apoptosis of tumor cells in nude mice was detected by TUNEL assay after treatment with IFN-alpha-2b.
  • RESULTS: Tumors were significantly smaller and had a lower weight in the IFN-alpha-2b treatment groups than those in the control group (P < 0.01), and the tumor growth inhibition rate in groups A, B and C was 27.78%, 65.22% and 49.64%, respectively.
  • The expression levels of both genes and proteins of COX-2 and VEGF were much lower in the IFN-alpha-2b treatment groups than in the control group (P < 0.01).
  • The apoptosis index (AI) of tumor cells in the IFN-alpha-2b treatment groups was markedly higher than that in the control group (P < 0.01).
  • Group B had a higher inhibition rate of tumor growth, a lower expression level of COX-2 and VEGF and a higher AI than groups A and C (P < 0.05), but there was no significant difference between groups A and C.
  • CONCLUSION: The inhibitory effects of IFN-alpha-2b on implanted tumor growth and apoptosis may be associated with the down-regulation of COX-2 and VEGF expression.
  • The medium dose of IFN-alpha-2b for inhibiting tumor growth is 20000 IU/d.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Cyclooxygenase 2 / metabolism. Interferon-alpha / pharmacology. Liver Neoplasms / drug therapy. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. RNA, Messenger / metabolism. Recombinant Proteins

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  • (PMID = 19058305.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 99210-65-8 / interferon alfa-2b; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ PMC2773874
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34. Pasqui AL, Di Renzo M, Auteri A, Federico G, Puccetti L: Increased TNF-alpha production by peripheral blood mononuclear cells in patients with Krabbe's disease: effect of psychosine. Eur J Clin Invest; 2007 Sep;37(9):742-5
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  • [Title] Increased TNF-alpha production by peripheral blood mononuclear cells in patients with Krabbe's disease: effect of psychosine.
  • BACKGROUND: Inflammatory and/or immune activation occurs both in animal models (twitcher mice) and in the brain of patients with Globoid cell leukodystrophy (GLD) or Krabbe's disease (KD).
  • MATERIALS AND METHODS: We studied cytokine production by peripheral blood mononuclear cells (PBMCs) isolated from four KD patients, diagnosed on the basis of clinical criteria.
  • Cells were cultured and stimulated with appropriate agents and the supernatants collected before and after the addition of psychosine.
  • Tumour necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and monocyte chemoattractant factor (MCP)-1) production was evaluated (ELISA method) and compared with a group of 10 normal subjects.
  • RESULTS: We found a significant increase of TNF-alpha release by PBMCs of KD patients compared with healthy subjects; TNF-alpha production was significantly increased after LPS addition.
  • Psychosine was able to induce a further significant increase (P < 0.05) only in cells obtained from KD patients and not from control subjects.
  • CONCLUSIONS: The increased TNF-alpha production permits us to confirm the presence of an inflammatory-immune stimulus in KD patients, which may be induced and potentiated by the pathogenetic metabolite psychosine.
  • [MeSH-major] Cytokines / metabolism. Leukodystrophy, Globoid Cell / etiology. Psychosine / adverse effects. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adult. Animals. Disease Models, Animal. Female. Humans. Male. Mice. Treatment Outcome

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  • [ErratumIn] Eur J Clin Invest. 2008 Apr;38(4):280
  • (PMID = 17696965.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 2238-90-6 / Psychosine
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35. Buscemi L, Ramonet D, Geiger JD: Human immunodeficiency virus type-1 protein Tat induces tumor necrosis factor-alpha-mediated neurotoxicity. Neurobiol Dis; 2007 Jun;26(3):661-70
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  • [Title] Human immunodeficiency virus type-1 protein Tat induces tumor necrosis factor-alpha-mediated neurotoxicity.
  • HIV-1 infection causes, with increasing prevalence, neurological disorders characterized in part by neuronal cell death.
  • Here, we tested the hypothesis that a non-neurotoxic epitope of Tat can, through actions on immune cells, increase neuronal cell death.
  • Tat(1-72) and a mutant Tat(1-72) lacking the neurotoxic epitope (Tat(Delta31-61)) concentration-dependently and markedly increased TNF-alpha production in macrophage-like differentiated human U937 and THP-1 cells, in mouse peritoneal macrophages and in mouse brain microglia.
  • Supernatants from U937 cells treated with either Tat(1-72) or Tat(Delta31-61) were neurotoxic and their immunoneutralization with an anti-TNF-alpha antibody decreased Tat(1-72)- and Tat(Delta31-61)-induced neurotoxicity.
  • Together, these results demonstrate that the neurotoxic epitope of Tat(1-72) is different from the epitope that is indirectly neurotoxic following production of TNF-alpha from immune cells, and suggest that therapeutic interventions against TNF-alpha might be beneficial against HIV-1 associated neurological disorders.

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  • (PMID = 17451964.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR17699; United States / NIA NIH HHS / AG / AG17628; United States / NCRR NIH HHS / RR / P20 RR017699-05; United States / NCRR NIH HHS / RR / P20 RR017699; United States / NCRR NIH HHS / RR / RR017699-05; United States / NIA NIH HHS / AG / P01 AG017628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes; 0 / Gene Products, tat; 0 / Neurotoxins; 0 / Tumor Necrosis Factor-alpha; 0 / tat Gene Products, Human Immunodeficiency Virus
  • [Other-IDs] NLM/ NIHMS25465; NLM/ PMC2080622
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36. Lo YT, Tzeng TF, Liu IM: Role of tumor suppressor PTEN in tumor necrosis factor alpha-induced inhibition of insulin signaling in murine skeletal muscle C2C12 cells. Horm Metab Res; 2007 Mar;39(3):173-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of tumor suppressor PTEN in tumor necrosis factor alpha-induced inhibition of insulin signaling in murine skeletal muscle C2C12 cells.
  • In an attempt to clarify the role of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in muscle insulin resistance, we investigated the effect of PTEN on phosphoinositide 3 (PI3)-kinase/Akt related insulin signaling pathway in skeletal muscle-like C2C12 cells damaged by tumor necrosis factor-alpha (TNFalpha).
  • C2C12 cells cultured with TNFalpha (10 ng/ml) for 1 h displayed a marked decrease of insulin-stimulated 2-[14C]-deoxy-D-glucose (2-DG) uptake in parallel with an elevation of PTEN mRNA and protein levels.
  • However, pretreatment of PTEN antisense oligonucleotide (AS) (1 micromol/l for 3 days) for specific inhibition of PTEN expression in C2C12 cells abolished the TNFalpha-induced changes in 2-DG uptake.
  • Data taken from cultured C2C12 cells emphasize the negative regulatory of muscle PI3-kinase/Akt signaling pathways as the major substrate of PTEN but also support the concept that PTEN contributes to the development of insulin resistance in skeletal muscle.
  • [MeSH-major] Insulin / metabolism. Muscle Fibers, Skeletal / drug effects. Muscle Fibers, Skeletal / metabolism. PTEN Phosphohydrolase / metabolism. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Line. Gene Expression Regulation / drug effects. Glucose / metabolism. Glucose Transporter Type 4 / metabolism. Mice. Oligonucleotides, Antisense / pharmacology. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 17373630.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glucose Transporter Type 4; 0 / Insulin; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Slc2a4 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; IY9XDZ35W2 / Glucose
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37. Sikora AG, Jaffarzad N, Hailemichael Y, Gelbard A, Stonier SW, Schluns KS, Frasca L, Lou Y, Liu C, Andersson HA, Hwu P, Overwijk WW: IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity. J Immunol; 2009 Jun 15;182(12):7398-407
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  • [Title] IFN-alpha enhances peptide vaccine-induced CD8+ T cell numbers, effector function, and antitumor activity.
  • Type I IFNs, including IFN-alpha, enhance Ag presentation and promote the expansion, survival, and effector function of CD8(+) CTL during viral infection.
  • Because these are ideal characteristics for a vaccine adjuvant, we examined the efficacy and mechanism of exogenous IFN-alpha as an adjuvant for antimelanoma peptide vaccination.
  • We studied the expansion of pmel-1 transgenic CD8(+) T cells specific for the gp100 melanocyte differentiation Ag after vaccination of mice with gp100(25-33) peptide in IFA.
  • IFN-alpha synergized with peptide vaccination in a dose-dependent manner by boosting relative and absolute numbers of gp100-specific T cells that suppressed B16 melanoma growth.
  • IFN-alpha dramatically increased the accumulation of gp100-specific, IFN-gamma-secreting, CD8(+) T cells in the tumor through reduced apoptosis and enhanced proliferation of Ag-specific CD8(+) T cells.
  • IFN-alpha treatment also greatly increased the long-term maintenance of pmel-1 CD8(+) T cells with an effector memory phenotype, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host.
  • These results demonstrate the efficacy of IFN-alpha as an adjuvant for peptide vaccination, give insight into its mechanism of action, and provide a rationale for clinical trials in which vaccination is combined with standard-of-care IFN-alpha therapy for melanoma.

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  • (PMID = 19494262.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIDCD NIH HHS / DC / T32 DC007367; United States / NIAID NIH HHS / AI / AI070910-03; United States / NIAID NIH HHS / AI / AI070910; United States / NIDCD NIH HHS / DC / DC007367-03; United States / NCI NIH HHS / CA / CA093459-030006; United States / NIDCD NIH HHS / DC / T32 DC007367-03; United States / NIAID NIH HHS / AI / R01 AI070910; United States / NIAID NIH HHS / AI / R01 AI070910-03; United States / NCI NIH HHS / CA / P50 CA093459-030006; United States / NCI NIH HHS / CA / P50 CA093459
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Interferon-alpha; 0 / Interleukin-15; 0 / Vaccines, Subunit; 156986-95-7 / Receptor, Interferon alpha-beta
  • [Other-IDs] NLM/ NIHMS121909; NLM/ PMC2774140
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38. Park SY, Choi JH, Ryu HS, Pak YK, Park KS, Lee HK, Lee W: C1q tumor necrosis factor alpha-related protein isoform 5 is increased in mitochondrial DNA-depleted myocytes and activates AMP-activated protein kinase. J Biol Chem; 2009 Oct 9;284(41):27780-9
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  • [Title] C1q tumor necrosis factor alpha-related protein isoform 5 is increased in mitochondrial DNA-depleted myocytes and activates AMP-activated protein kinase.
  • Here we show that the expression of C1q tumor necrosis factor alpha-related protein isoform 5 (C1QTNF5) is drastically increased following depletion of mtDNA in myocytes.
  • Similar to adiponectin, C1QTNF5 induced the phosphorylation of AMP-activated protein kinase (AMPK), leading to increased cell surface recruitment of GLUT4 and increased glucose uptake.
  • Treatment of cells with purified recombinant C1QTNF5 increased the phosphorylation of acetyl-CoA carboxylase and stimulated fatty acid oxidation.
  • [MeSH-major] AMP-Activated Protein Kinases / metabolism. DNA, Mitochondrial. Intracellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / metabolism. Muscle Cells
  • [MeSH-minor] Acetyl-CoA Carboxylase / genetics. Acetyl-CoA Carboxylase / metabolism. Aminoimidazole Carboxamide / analogs & derivatives. Aminoimidazole Carboxamide / metabolism. Animals. Cell Line. Collagen / genetics. Collagen / metabolism. Diabetes Mellitus, Type 2 / metabolism. Disease Models, Animal. Enzyme Activation. Fatty Acids / metabolism. Glucose / metabolism. Glucose Transporter Type 4 / genetics. Glucose Transporter Type 4 / metabolism. Humans. Insulin Receptor Substrate Proteins / genetics. Insulin Receptor Substrate Proteins / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Obese. Mitochondria / genetics. Mitochondria / metabolism. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rats. Rats, Inbred OLETF. Receptors, Adiponectin / genetics. Receptors, Adiponectin / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Ribonucleotides / genetics. Ribonucleotides / metabolism. p38 Mitogen-Activated Protein Kinases / genetics. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19651784.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C1QTNF5 protein, human; 0 / C1QTNF5 protein, rat; 0 / CTRP5 protein, mouse; 0 / DNA, Mitochondrial; 0 / Fatty Acids; 0 / Glucose Transporter Type 4; 0 / Insulin Receptor Substrate Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Irs1 protein, rat; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Adiponectin; 0 / Recombinant Fusion Proteins; 0 / Ribonucleotides; 0 / Slc2a4 protein, rat; 0 / adiponectin receptor 1, rat; 0 / adiponectin receptor 2, rat; 360-97-4 / Aminoimidazole Carboxamide; 9007-34-5 / Collagen; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 6.4.1.2 / Acetyl-CoA Carboxylase; F0X88YW0YK / AICA ribonucleotide; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2788828
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39. Wilkes JJ, Lloyd DJ, Gekakis N: Loss-of-function mutation in myostatin reduces tumor necrosis factor alpha production and protects liver against obesity-induced insulin resistance. Diabetes; 2009 May;58(5):1133-43
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  • [Title] Loss-of-function mutation in myostatin reduces tumor necrosis factor alpha production and protects liver against obesity-induced insulin resistance.
  • To evaluate postprandial insulin sensitivity between animals of a similar size, glucose and insulin tolerance tests and hyperinsulinemic-euglycemic clamp studies were performed with heterozygous and homozygous mutant mice.
  • Improvements to muscle and liver insulin sensitivity (approximately 200-400%) correlated with 50-75% decreased tumor necrosis factor (TNF)alpha production and coincided with severe Mstn deficiency.
  • [MeSH-major] Dietary Fats / pharmacology. Glucose / metabolism. Insulin Resistance / physiology. Liver / physiology. Metabolic Syndrome X / prevention & control. Mutation. Myostatin / genetics. Obesity / physiopathology. Tumor Necrosis Factor-alpha / biosynthesis


40. Ajit D, Udan ML, Paranjape G, Nichols MR: Amyloid-beta(1-42) fibrillar precursors are optimal for inducing tumor necrosis factor-alpha production in the THP-1 human monocytic cell line. Biochemistry; 2009 Sep 29;48(38):9011-21
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  • [Title] Amyloid-beta(1-42) fibrillar precursors are optimal for inducing tumor necrosis factor-alpha production in the THP-1 human monocytic cell line.
  • Pathological studies have determined that fibrillar forms of amyloid-beta protein (Abeta) comprise the characteristic neuritic plaques in Alzheimer's disease (AD).
  • Although the plaques are a hallmark of AD, they are only part of an array of Abeta aggregate morphologies observed in vivo.
  • An aliquot of freshly reconstituted Abeta(1-42) in sterile water (100 microM, pH 3.6) did not effectively stimulate the cells at a final Abeta concentration of 15 microM.
  • However, quiescent incubation of the peptide at 4 degrees C for 48-96 h greatly enhanced its ability to induce tumor necrosis factor-alpha (TNFalpha) production, the level of which surprisingly declined upon further aggregation.
  • Imaging of the Abeta(1-42) aggregation solutions with atomic force microscopy indicated that the best cellular response coincided with the appearance of fibrillar structures, yet conditions that accelerated or increased the level of Abeta(1-42) fibril formation such as peptide concentration, temperature, or reconstitution in NaOH/PBS at pH 7.4 diminished its ability to stimulate the cells.

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  • (PMID = 19694428.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG033913-01; United States / NIA NIH HHS / AG / R15 AG033913; United States / NIA NIH HHS / AG / R15 AG033913-01; United States / NIA NIH HHS / AG / R15AG033913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Inflammation Mediators; 0 / Peptide Fragments; 0 / Protein Precursors; 0 / Tumor Necrosis Factor-alpha; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42)
  • [Other-IDs] NLM/ NIHMS143126; NLM/ PMC2749082
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41. Baron MJ, Filman DJ, Prophete GA, Hogle JM, Madoff LC: Identification of a glycosaminoglycan binding region of the alpha C protein that mediates entry of group B Streptococci into host cells. J Biol Chem; 2007 Apr 6;282(14):10526-36
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  • [Title] Identification of a glycosaminoglycan binding region of the alpha C protein that mediates entry of group B Streptococci into host cells.
  • The alpha C protein (ACP) on the surface of GBS contributes to this process.
  • A virulence factor in mouse models of infection, and prototype for a family of Gram-positive bacterial surface proteins, ACP facilitates GBS entry into human cervical epithelial cells and movement across cell layers.
  • ACP binds to host cell surface glycosaminoglycan (GAG).
  • From crystallography, we have identified a cluster of basic residues (BR2) that is a putative GAG binding area in Domain 2, near the junction of the N-terminal domain of ACP and the first of a series of tandem amino acid repeats.
  • D2-R, a protein construct including this region, binds to cells similarly to full-length ACP.
  • We now demonstrate that the predicted charged BR2 residues confer GAG binding; site-directed mutagenesis of these residues (Arg(172), Arg(185), or Lys(196)) eliminates cell-binding activity of construct D2-R.
  • This strain enters host cells less effectively than does the wild-type strain and similarly to an ACP null mutant strain.
  • GBS entry into host cells and transcytosis of host cells may occur by distinct mechanisms.

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  • (PMID = 17259175.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ AAA26848/ M97256
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020566; United States / NIAID NIH HHS / AI / AI059495; United States / NIAID NIH HHS / AI / AI38424
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Bacterial Proteins; 0 / Glycosaminoglycans; 0 / Virulence Factors; 149025-02-5 / alpha C protein, group B streptococci
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42. Mathsson L, Tejde A, Carlson K, Höglund M, Nilsson B, Nilsson-Ekdahl K, Rönnelid J: Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones. Br J Haematol; 2005 Jun;129(6):830-8
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  • [Title] Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones.
  • In accordance with our findings of IC-induced cytokine production from peripheral blood mononuclear cells (PBMC) in systemic lupus erythematosus, we investigated whether CG can also induce cytokine production.
  • Complement blockade resulted in increased IgG CG-induced interleukin (IL)-10 production that was inversely correlated with decreased production of tumour necrosis factor-alpha.
  • [MeSH-minor] Aged. Cells, Cultured. Complement Inactivator Proteins / immunology. Complement Pathway, Classical / immunology. Female. Humans. Hydrogen-Ion Concentration. Immunoglobulin G / immunology. Immunoglobulin M / immunology. Interleukin-10 / biosynthesis. Male. Middle Aged. Monocytes / immunology. Neoplastic Stem Cells / pathology. Temperature. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 15953012.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Complement Inactivator Proteins; 0 / Cryoglobulins; 0 / Cytokines; 0 / Fc gamma receptor IIA; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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43. Reynolds JL, Ignatowski TA, Spengler RN: Effect of tumor necrosis factor-alpha on the reciprocal G-protein-induced regulation of norepinephrine release by the alpha2-adrenergic receptor. J Neurosci Res; 2005 Mar 15;79(6):779-87
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  • [Title] Effect of tumor necrosis factor-alpha on the reciprocal G-protein-induced regulation of norepinephrine release by the alpha2-adrenergic receptor.
  • Alpha2-adrenergic receptors control norepinephrine (NE) release and tumor necrosis factor-alpha (TNF) production from neurons.
  • [MeSH-major] GTP-Binding Proteins / physiology. Guanosine Triphosphate / analogs & derivatives. Hippocampus / drug effects. Norepinephrine / secretion. Receptors, Adrenergic, alpha-2 / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Adrenergic alpha-Agonists / pharmacology. Adrenergic alpha-Antagonists / pharmacology. Animals. Azides / pharmacology. Brimonidine Tartrate. Cell Membrane / drug effects. Cell Membrane / radiation effects. Dose-Response Relationship, Drug. Drug Interactions. Electrophoresis, Polyacrylamide Gel / methods. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. In Vitro Techniques. Male. Pertussis Toxin / pharmacology. Phenoxybenzamine / pharmacology. Phosphorus Isotopes / pharmacology. Quinoxalines / pharmacology. Rats. Rats, Sprague-Dawley. Yohimbine / pharmacology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15672410.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS41352
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-Agonists; 0 / Adrenergic alpha-Antagonists; 0 / Azides; 0 / Phosphorus Isotopes; 0 / Quinoxalines; 0 / Receptors, Adrenergic, alpha-2; 0 / Tumor Necrosis Factor-alpha; 0TTZ664R7Z / Phenoxybenzamine; 2Y49VWD90Q / Yohimbine; 4S9CL2DY2H / Brimonidine Tartrate; 60869-76-3 / GTP gamma-4-azidoanilide; 86-01-1 / Guanosine Triphosphate; EC 2.4.2.31 / Pertussis Toxin; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11; X4W3ENH1CV / Norepinephrine
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44. Chen QY, Jiang ZY, Wu LJ, Zhang BY, Lu GH, Zhou JY: [Expression of alpha-tubulin and MDR1 and their correlation with the biological features of non-small cell lung carcinoma]. Zhonghua Zhong Liu Za Zhi; 2010 Apr;32(4):278-82
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  • [Title] [Expression of alpha-tubulin and MDR1 and their correlation with the biological features of non-small cell lung carcinoma].
  • OBJECTIVE: To detect the expression of alpha-tubulin and MDR1 in human non-small cell lung carcinoma (NSCLC), and to clarify their clinical significance.
  • METHODS: Paraffin embedded tissues from 158 primary non-small lung carcinomas and 30 paracancerous lung tissues were examined for expression of alpha-tubulin and MDR1 by immunohistochemistry (SP method).
  • The relationship between alpha-tubulin and MDR1 expression and the biological features of lung carcinoma was analyzed.
  • RESULTS: The positive rate of alpha-tubulin and MDR1 expressions in the lung carcinomas was 65.2% and 51.3%, respectively.
  • Western blot analysis showed that the level of alpha-tubulin and MDR1 expressions in NSCLC tissues were 0.49 +/- 0.06 and 0.56 +/- 0.04, respectively, significantly higher than that in paracancerous tissues (0.07 +/- 0.01) (t = 3.693 and t = 6.769, P < 0.01).
  • The positive rate of alpha-tubulin expression was gradually increased with tumor progression, significantly higher in III-IV stage cancers and in poorly differentiated carcinomas (both P < 0.01).
  • The positive rate of alpha-tubulin in well-moderately differentiated carcinomas was lower than that in poorly differentiated ones.
  • There was no significant correlation with age, sex, tumor size, histological type, clinical TNM system and lymph node metastasis.
  • The positive rate of MDR1 was not correlated with sex, age, tumor size, pathological grading, clinical TNM stages and lymph node metastasis.
  • But the positive rate of MDR1 in adenocarcinoma was significantly higher than that in squamous carcinoma and undifferentiated large cell carcinomas (P < 0.01).
  • alpha-tubulin and MDR1 expression had no impact on the outcome of chemotherapy (chi(2) = 0.69 and 1.30, P > 0.05, respectively).
  • Univariate analysis showed that the 5-year survival rate of patients with negative alpha-tubulin and MDR1 expression was 30.7% and 28.5%, respectively, significantly higher than that of patients with positive alpha-tubulin and MDR1 expression (13.5% and 11.8%, respectively) (chi(2) = 20.69 and 15.52, P < 0.01, respectively), and multivariate Cox regression analysis showed that alpha-tubulin (RR = 3.287, P = 0.006) and clinical TNM stage (RR = 1.954, P = 0.025) were significantly independent predictive factor for patients with lung cancer, MDR1 and other factors could not be used as an independent predicitive factors.
  • However, there was no significant correlation between the expression of alpha-tubulin and MDR1 in lung carcinoma(r = 0.093, P > 0.05).
  • CONCLUSION: The expression of alpha-tubulin and MDR1 may play an important role in the development and progression of human non-small cell lung carcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. P-Glycoprotein / metabolism. Tubulin / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Female. Gene Expression Regulation, Neoplastic. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. P-Glycoproteins. Paraffin Embedding. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Proportional Hazards Models. Survival Rate

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  • (PMID = 20510079.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / TUBA1A protein, human; 0 / Tubulin
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45. Crippa L, Gasparri A, Sacchi A, Ferrero E, Curnis F, Corti A: Synergistic damage of tumor vessels with ultra low-dose endothelial-monocyte activating polypeptide-II and neovasculature-targeted tumor necrosis factor-alpha. Cancer Res; 2008 Feb 15;68(4):1154-61
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  • [Title] Synergistic damage of tumor vessels with ultra low-dose endothelial-monocyte activating polypeptide-II and neovasculature-targeted tumor necrosis factor-alpha.
  • High-dose endothelial-monocyte activating polypeptide II (EMAP-II), a tumor-derived antiangiogenic cytokine, can sensitize tumor vasculature to the damaging activity of high-dose tumor necrosis factor (TNF)-alpha.
  • Coadministration of 0.1 ng of EMAP-II and 0.1 ng of CNGRCG-TNF (NGR-TNF), a peptide-TNF conjugate able to target tumor blood vessels, inhibited lymphoma and melanoma growth in mice, with no evidence of toxicity.
  • This drug combination induced endothelial cell apoptosis in vivo and, at later time points, caused reduction of vessel density and massive apoptosis of tumor cells.
  • Tumor vascular targeting with extremely low amounts of these cytokines may represent a new strategy for cancer treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cytokines / pharmacology. Neoplasm Proteins / pharmacology. RNA-Binding Proteins / pharmacology. Recombinant Fusion Proteins / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Endothelial Cells / drug effects. Endothelial Cells / pathology. Humans. Lymphoma / drug therapy. Melanoma, Experimental / blood supply. Melanoma, Experimental / drug therapy. Mice. Mice, Inbred C57BL. Receptors, Tumor Necrosis Factor, Type I / metabolism. Recombinant Proteins / pharmacology

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  • (PMID = 18281491.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / small inducible cytokine subfamily E, member 1; 0 / tumor Necrosis Factor-alpha, CNGRC fusion protein, mouse; 0 / tumor necrosis factor-alpha, CNGRC fusion protein, human
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46. Romano A, Adriaens M, Kuenen S, Delvoux B, Dunselman G, Evelo C, Groothuis P: Identification of novel ER-alpha target genes in breast cancer cells: gene- and cell-selective co-regulator recruitment at target promoters determines the response to 17beta-estradiol and tamoxifen. Mol Cell Endocrinol; 2010 Jan 15;314(1):90-100
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  • [Title] Identification of novel ER-alpha target genes in breast cancer cells: gene- and cell-selective co-regulator recruitment at target promoters determines the response to 17beta-estradiol and tamoxifen.
  • Tamoxifen and 17beta-estradiol are capable of up-regulating the expression of some genes and down-regulate the expression of others simultaneously in the same cell.
  • To elucidate whether these events are determined by differences in the recruitment of co-regulators by activated estrogen receptor-alpha (ER-alpha) at target promoters, we applied chromatin immunoprecipitation (ChIP) with promoter microarray hybridisation in breast cancer T47D cells and identified 904 ER-alpha targets genome-wide.
  • This is shown for both breast (T47D) and endometrial carcinoma cells (ECC1).
  • Moreover, differential co-regulator recruitment also explains that tamoxifen regulates a number of genes in opposite direction in breast and endometrial cancer cells.
  • Our findings support the notion that recruitment of co-regulator at target gene promoters and their expression levels determine the effect of ER-alpha on gene expression to a large extent.
  • [MeSH-major] Antineoplastic Agents, Hormonal. Breast Neoplasms. Estradiol / pharmacology. Estrogen Receptor alpha / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Promoter Regions, Genetic. Tamoxifen
  • [MeSH-minor] Cell Line, Tumor. Female. Humans. Nuclear Receptor Co-Repressor 2 / genetics. Nuclear Receptor Co-Repressor 2 / metabolism. Transcription, Genetic

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  • (PMID = 19698761.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Receptor alpha; 0 / NCOR2 protein, human; 0 / Nuclear Receptor Co-Repressor 2; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol
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47. Kumar S, Singh BK, Pandey AK, Kumar A, Sharma SK, Raj HG, Prasad AK, Van der Eycken E, Parmar VS, Ghosh B: A chromone analog inhibits TNF-alpha induced expression of cell adhesion molecules on human endothelial cells via blocking NF-kappaB activation. Bioorg Med Chem; 2007 Apr 15;15(8):2952-62
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  • [Title] A chromone analog inhibits TNF-alpha induced expression of cell adhesion molecules on human endothelial cells via blocking NF-kappaB activation.
  • The interaction between leukocytes and the vascular endothelial cells (EC) via cellular adhesion molecules plays an important role in various inflammatory and immune diseases.
  • In an effort to develop potent cell adhesion molecule inhibitors, a series of chromone derivatives bearing alkoxycarbonylvinyl unit at the C-3 position, that is, the chromones 8a-d and 9a-d, were designed and synthesized, and evaluated for their ICAM-1 inhibitory activity on human endothelial cells as well as their effect on NADPH-catalyzed rat microsomal lipid peroxidation.
  • Further, we found that incorporation of unsaturation in the alcohol moiety increases the potential of the compound for the inhibition of TNF-alpha induced expression of ICAM-1 and also for the inhibition of lipid peroxidation.
  • We have found that compound 8a also significantly inhibited the TNF-alpha induced expression of VCAM-1 and E-selectin, which play key roles in various inflammatory diseases.
  • The functional consequences of inhibiting cell adhesion molecules were studied by performing cell-adhesion assay.
  • To elucidate the molecular mechanism of inhibition of cell adhesion molecules, we investigated the status of nuclear transcription factor-kappaB (NF-kappaB) and were able to establish that compound 8a significantly blocked the TNF-alpha induced activation of NF-kappaB.
  • [MeSH-major] Cell Adhesion Molecules / biosynthesis. Chromones / chemical synthesis. Chromones / pharmacology. Endothelial Cells / metabolism. NF-kappa B / metabolism. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Biotransformation / drug effects. Blotting, Western. Cell Adhesion / drug effects. Cell Line. Cell Survival / drug effects. Cells, Cultured. Drug Design. E-Selectin / biosynthesis. Flow Cytometry. Humans. In Vitro Techniques. Indicators and Reagents. Intercellular Adhesion Molecule-1 / biosynthesis. Lipid Peroxidation / drug effects. Microsomes, Liver / drug effects. Microsomes, Liver / metabolism. NADP / metabolism. Neutrophils / drug effects. Rats. Spectrometry, Mass, Electrospray Ionization. Spectrophotometry, Infrared. Spectrophotometry, Ultraviolet. Structure-Activity Relationship. Transcription Factor RelA / biosynthesis. Tubulin / biosynthesis. Vascular Cell Adhesion Molecule-1 / biosynthesis

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  • (PMID = 17321745.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Chromones; 0 / E-Selectin; 0 / Indicators and Reagents; 0 / NF-kappa B; 0 / Transcription Factor RelA; 0 / Tubulin; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 53-59-8 / NADP
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48. Smoak K, Cidlowski JA: Glucocorticoids regulate tristetraprolin synthesis and posttranscriptionally regulate tumor necrosis factor alpha inflammatory signaling. Mol Cell Biol; 2006 Dec;26(23):9126-35
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  • [Title] Glucocorticoids regulate tristetraprolin synthesis and posttranscriptionally regulate tumor necrosis factor alpha inflammatory signaling.
  • Here we report that glucocorticoids induce the synthesis of TTP mRNA and protein in A549 lung epithelial cells and in rat tissues.
  • The most widely characterized TTP-regulated gene is the AU-rich tumor necrosis factor alpha (TNF-alpha) gene.
  • Dexamethasone represses TNF-alpha mRNA in A549 cells and decreases luciferase expression of a TNF-alpha 3' untranslated region reporter plasmid in an orientation-dependent manner.
  • Small interfering RNAs to TTP significantly prevent this effect, and a cell line stably expressing a short-hairpin RNA to TTP conclusively establishes that TTP is critical for dexamethasone inhibition of TNF-alpha mRNA expression.

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  • (PMID = 16982682.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Tristetraprolin; 0 / Tumor Necrosis Factor-alpha; 7S5I7G3JQL / Dexamethasone; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC1636823
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49. Murata Y, Olmarker K, Larsson K, Takahashi K, Rydevik B: Production of tumor necrosis factor-alpha from porcine nucleus pulposus cells at various time points in cell culture under conditions of nutritional deficiency. Cytokine; 2006 May;34(3-4):206-11
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  • [Title] Production of tumor necrosis factor-alpha from porcine nucleus pulposus cells at various time points in cell culture under conditions of nutritional deficiency.
  • NP has been shown to be capable of producing tumor necrosis factor-alpha (TNF).
  • NP cells were cultured and processed for immunohistochemistry using antisera to TNF, and for ELISA to measure TNF production.
  • [MeSH-major] Ganglia, Spinal / cytology. Ganglia, Spinal / metabolism. Malnutrition / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Cell Culture Techniques. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Intervertebral Disc Displacement. Lumbar Vertebrae. Swine. Time Factors

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  • (PMID = 16766205.001).
  • [ISSN] 1043-4666
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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50. Dinh C, Hoang K, Haake S, Chen S, Angeli S, Nong E, Eshraghi AA, Balkany TJ, Van De Water TR: Biopolymer-released dexamethasone prevents tumor necrosis factor alpha-induced loss of auditory hair cells in vitro: implications toward the development of a drug-eluting cochlear implant electrode array. Otol Neurotol; 2008 Oct;29(7):1012-9
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  • [Title] Biopolymer-released dexamethasone prevents tumor necrosis factor alpha-induced loss of auditory hair cells in vitro: implications toward the development of a drug-eluting cochlear implant electrode array.
  • HYPOTHESIS: Polymer-eluted dexamethasone (DXM) will retain its ability to protect against tumor necrosis factor alpha (TNFalpha)-induced hair cell (HC) loss.
  • [MeSH-major] Cochlear Implants. Delayed-Action Preparations / pharmacology. Dexamethasone / pharmacology. Hair Cells, Auditory / physiology. Hearing Loss / prevention & control. Organ of Corti / drug effects. Prosthesis Design. Tumor Necrosis Factor-alpha / adverse effects

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  • (PMID = 18818545.001).
  • [ISSN] 1537-4505
  • [Journal-full-title] Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
  • [ISO-abbreviation] Otol. Neurotol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biopolymers; 0 / Delayed-Action Preparations; 0 / Tumor Necrosis Factor-alpha; 7S5I7G3JQL / Dexamethasone
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51. Wang Z, Bryan J, Franz C, Havlioglu N, Sandell LJ: Type IIB procollagen NH(2)-propeptide induces death of tumor cells via interaction with integrins alpha(V)beta(3) and alpha(V)beta(5). J Biol Chem; 2010 Jul 2;285(27):20806-17
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  • [Title] Type IIB procollagen NH(2)-propeptide induces death of tumor cells via interaction with integrins alpha(V)beta(3) and alpha(V)beta(5).
  • Cartilage is resistant to tumor invasion.
  • In the present study, we found that the NH(2)-propeptide of the cartilage-characteristic collagen, type IIB, PIIBNP, is capable of killing tumor cells.
  • This peptide adheres to and kills cells from chondrosarcoma and cervical and breast cancer cell lines via the integrins alpha(v)beta(5) and alpha(v)beta(3).
  • Adhesion is abrogated by blocking with anti alpha(v)beta(5) and alpha(v)beta(3) antibodies.
  • When alpha(v) is suppressed by small intefering RNA, adhesion and cell killing are blocked.
  • Normal chondrocytes from developing cartilage do not express alpha(v)beta(3) and alpha(v)beta(5) integrins and are thus protected from cell death.
  • Morphological, DNA, and biochemical evidence indicates that the cell death is not by apoptosis but probably by necrosis.
  • In an assay for invasion, PIIBNP reduced the number of cells crossing the membrane.
  • In vivo, in a tumor model for breast cancer, PIIBNP was consistently able to reduce the size of the tumor.

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  • (PMID = 20439458.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P30 AR057235; United States / NIAMS NIH HHS / AR / R01 AR036994; United States / NIAMS NIH HHS / AR / R01 AR050847; United States / NIAMS NIH HHS / AR / R01 AR R01 036994
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Ribosomal; 0 / Integrin alphaVbeta3; 0 / Peptide Fragments; 0 / Procollagen; 0 / Receptors, Vitronectin; 0 / integrin alphaVbeta5; 63231-63-0 / RNA
  • [Other-IDs] NLM/ PMC2898354
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52. Ma Y, Zhao J, Yang S, Jia Y: [Cigu Xiaozhi pills's influence on lipid peroxidation and TNF-alpha expression in liver tissues of rats with nonalcoholic steatohepatitis]. Zhongguo Zhong Yao Za Zhi; 2010 May;35(10):1292-7
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  • [Title] [Cigu Xiaozhi pills's influence on lipid peroxidation and TNF-alpha expression in liver tissues of rats with nonalcoholic steatohepatitis].
  • OBJECTIVE: To investigate the effect of Cigu Xiaozhi pills on expression of tumor necrosis factor alpha (TNF-alpha) in rat with nonalcoholic steatoheptatitis (NASH).
  • The expression of TNF-alpha in the liver was determined using the immunohistochemical technique and RT-PCR.
  • RESULT: In model group, extensive adipose degeneration and inflammatory cell infiltration were found in the liver.
  • TNF-alpha was not expressed almost in normal rat liver and was expressed highly in model rat liver.
  • Compared with model group, the TNF-alpha mRNA and protein expression were significantly lower in liver of treatment groups and positive control group (P < 0.05).
  • CONCLUSION: TNF-alpha plays an important role in NASH pathogenesis.
  • [MeSH-major] Drugs, Chinese Herbal / administration & dosage. Fatty Liver / drug therapy. Fatty Liver / metabolism. Lipid Peroxidation / drug effects. Liver / metabolism. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Gene Expression / drug effects. Humans. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 20707200.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Tumor Necrosis Factor-alpha
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53. Prabhu Anand S, Selvaraj P, Narayanan PR: Effect of 1,25 dihydroxyvitamin D3 on intracellular IFN-gamma and TNF-alpha positive T cell subsets in pulmonary tuberculosis. Cytokine; 2009 Feb;45(2):105-10
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  • [Title] Effect of 1,25 dihydroxyvitamin D3 on intracellular IFN-gamma and TNF-alpha positive T cell subsets in pulmonary tuberculosis.
  • We studied the immunomodulatory effect of 1,25(OH)(2)D(3) on single cell expression of IFN-gamma and TNF-alpha cytokines in T cell subsets of pulmonary tuberculosis (PTB) patients (n=22) and normal healthy subjects (n=22).
  • Peripheral blood mononuclear cells (PBMCs) were cultured with live Mycobacterium tuberculosis (MTB) with or without 1,25(OH)(2)D(3) (10(-7)M) for 48 h.
  • T cell subsets positive for IFN-gamma and TNF-alpha were enumerated by flow cytometry and the culture supernatants were assayed for both the cytokines using ELISA.
  • In both NHS and PTB patients, a significantly reduced percentage of IFN-gamma and TNF-alpha expressing CD3+, CD3+CD4+ and CD3+CD8+ T cells were observed in cultures stimulated with live MTB and treated with 1,25(OH)(2)D(3) compared to cultures without 1,25(OH)(2)D(3) (NHS; CD3+ IFN-gamma+: p<0.0001; CD3+TNF-alpha+: p=0.0292 and PTB; CD3+ IFN-gamma+: p=0.0292; CD3+ TNF-alpha+: p=0.0028).
  • The levels of IFN-gamma and TNF-alpha in the culture supernatants of 1,25(OH)(2)D(3) treated cultures were also found to be significantly decreased in both groups (NHS; IFN-gamma: p=0.0001; TNF-alpha: p<0.0001) and (PTB; IFN-gamma: p<0.0001; TNF-alpha: p<0.0001).
  • A positive correlation was observed between IFN-gamma and TNF-alpha expressing CD3+CD8+ T cells in MTB stimulated cultures treated with or without 1,25(OH)(2)D(3) in NHS (p=0.0001; p=0.001, respectively) and PTB patients (p=0.002; p=0.005, respectively).
  • The present study revealed the suppressive effect of 1,25(OH)(2)D(3) on single cell expression of IFN-gamma and TNF-alpha by CD3+CD4+ and CD3+CD8+ T cells in pulmonary tuberculosis.
  • This suppressive effect of 1,25(OH)(2)D(3) on proinflammatory and Th1 cytokine positive cells might have a role in reducing inflammation at the site of infection.
  • [MeSH-major] Calcitriol / pharmacology. Interferon-gamma / immunology. T-Lymphocyte Subsets. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. Tuberculosis, Pulmonary / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Adult. Animals. Antigens, CD / immunology. Cells, Cultured. Female. Humans. Lymphocyte Activation / immunology. Male. Mycobacterium tuberculosis / immunology

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  • (PMID = 19091593.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; FXC9231JVH / Calcitriol
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54. Nishikawa H, Kato T, Hirayama M, Orito Y, Sato E, Harada N, Gnjatic S, Old LJ, Shiku H: Regulatory T cell-resistant CD8+ T cells induced by glucocorticoid-induced tumor necrosis factor receptor signaling. Cancer Res; 2008 Jul 15;68(14):5948-54
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  • [Title] Regulatory T cell-resistant CD8+ T cells induced by glucocorticoid-induced tumor necrosis factor receptor signaling.
  • We previously found that a Salmonella typhimurium vector engineered to secrete soluble tumor antigen induces CD4(+) T cells resistant to CD4(+)CD25(+) regulatory T cells (Treg) and that glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) signal is involved in the development of this resistance.
  • Coadministration with GITRL during primary and secondary immunization enhanced the induction of mERK-specific CD8(+) T cells.
  • Antibody depletion and minigene analysis suggested that GITRL directly activated CTL epitope-specific CD8(+) T cells independently of CD4(+) T cells.
  • Immunization with plasmids encoding a CTL epitope and GITRL resulted in strong tumor inhibition in a CD8(+) T cell-dependent manner.
  • Furthermore, CTL epitope-specific CD8(+) T cells induced by immunization with plasmids encoding CTL epitope coadministered with GITRL were refractory to suppression by CD4(+)CD25(+) Tregs compared with CD8(+) T cells induced without GITR signaling.
  • We propose that coadministration of GITR signaling agents with tumor antigens constitutes a promising novel strategy for cancer vaccine development.
  • [MeSH-major] CD8-Positive T-Lymphocytes / cytology. Glucocorticoids / metabolism. T-Lymphocytes, Regulatory / metabolism. Tumor Necrosis Factors / metabolism
  • [MeSH-minor] Animals. Epitopes / chemistry. Female. Genetic Vectors. Interleukin-2 Receptor alpha Subunit / biosynthesis. Mice. Mice, Inbred BALB C. Mitogen-Activated Protein Kinase 1 / metabolism. Models, Biological. Plasmids / metabolism. Signal Transduction

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  • (PMID = 18632650.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes; 0 / Glucocorticoids; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factors; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1
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55. Jarvis MA, Borton JA, Keech AM, Wong J, Britt WJ, Magun BE, Nelson JA: Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. J Virol; 2006 Jun;80(11):5588-98
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  • [Title] Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation.
  • Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha).
  • In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways.
  • The effect on these pathways was limited to cells infected with the virus, occurred at late times of infection, and was independent of cell type or virus strain.
  • IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha.
  • The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation.
  • Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways.
  • We believe that the ability of HCMV to inhibit these two major proinflammatory pathways reveals a critical aspect of HCMV biology, with possible importance for immune evasion, as well as establishment of infection in cell types persistently infected by this virus.

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  • (PMID = 16699040.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI035602; United States / NIAID NIH HHS / AI / AI 21640; United States / NIAID NIH HHS / AI / AI 059335; United States / NIAID NIH HHS / AI / R01 AI021640; United States / NIAID NIH HHS / AI / AI 35602
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1472148
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56. Sakimoto T, Yamada A, Kanno H, Sawa M: Upregulation of tumor necrosis factor receptor 1 and TNF-alpha converting enzyme during corneal wound healing. Jpn J Ophthalmol; 2008 Sep-Oct;52(5):393-8
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  • [Title] Upregulation of tumor necrosis factor receptor 1 and TNF-alpha converting enzyme during corneal wound healing.
  • PURPOSE: To elucidate tumor necrosis factor (TNF) receptor-1 (TNFR1) and TNF-alpha converting enzyme (TACE) involvement during corneal wound healing.
  • Using cultured fibroblasts (human) and macrophages (mice), we evaluated the release of soluble TNF-alpha (sTNF-alpha) and soluble TNFR1 (sTNFR1) in the supernatant by enzyme-linked immunosorbent assay after stimulating TACE activity with phorbol myristate acetate (PMA).
  • RESULTS: In alkali-burned corneas, both TACE and TNFR1 expression were observed in the stromal cells after the acute phase of wound healing response.
  • In macrophage-cultured supernatant, both sTNF-alpha and sTNFR1 release were promoted by PMA stimulation.
  • [MeSH-major] ADAM Proteins / metabolism. Burns, Chemical / metabolism. Cornea / metabolism. Eye Burns / chemically induced. Receptors, Tumor Necrosis Factor, Type I / metabolism. Wound Healing / physiology
  • [MeSH-minor] ADAM17 Protein. Animals. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Fibroblasts / drug effects. Fibroblasts / metabolism. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Mice, Inbred BALB C. Sodium Hydroxide. Tetradecanoylphorbol Acetate / pharmacology. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation

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  • (PMID = 18991041.001).
  • [ISSN] 0021-5155
  • [Journal-full-title] Japanese journal of ophthalmology
  • [ISO-abbreviation] Jpn. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tnfrsf1a protein, mouse; 0 / Tumor Necrosis Factor-alpha; 55X04QC32I / Sodium Hydroxide; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.86 / ADAM17 Protein; EC 3.4.24.86 / ADAM17 protein, human; EC 3.4.24.86 / Adam17 protein, mouse; NI40JAQ945 / Tetradecanoylphorbol Acetate
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57. Cheng JD, Valianou M, Canutescu AA, Jaffe EK, Lee HO, Wang H, Lai JH, Bachovchin WW, Weiner LM: Abrogation of fibroblast activation protein enzymatic activity attenuates tumor growth. Mol Cancer Ther; 2005 Mar;4(3):351-60
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  • [Title] Abrogation of fibroblast activation protein enzymatic activity attenuates tumor growth.
  • Tumor-associated fibroblasts are functionally and phenotypically distinct from normal fibroblasts that are not in the tumor microenvironment.
  • Fibroblast activation protein is a 95 kDa cell surface glycoprotein expressed by tumor stromal fibroblasts, and has been shown to have dipeptidyl peptidase and collagenase activity.
  • Site-directed mutagenesis at the catalytic site of fibroblast activation protein, Ser624 --> Ala624, resulted in an approximately 100,000-fold loss of fibroblast activation protein dipeptidyl peptidase (DPP) activity.
  • HEK293 cells transfected with wild-type fibroblast activation protein, enzymatic mutant (S624A) fibroblast activation protein, or vector alone, were inoculated subcutaneously into immunodeficient mouse to assess the contribution of fibroblast activation protein enzymatic activity to tumor growth.
  • HEK293 cells transfected with fibroblast activation protein S624A showed tumor growth rates and tumorigenicity potential similar only to vector-transfected HEK293.
  • In vivo assessment of fibroblast activation protein DPP activity of these tumors showed enhanced enzymatic activity of wild-type fibroblast activation protein, with only baseline levels of fibroblast activation protein DPP activity in either fibroblast activation protein S624A or vector-only xenografts.
  • These results indicate that the enzymatic activity of fibroblast activation protein is necessary for fibroblast activation protein-driven tumor growth in the HEK293 xenograft model system.
  • This establishes the proof-of-principle that the enzymatic activity of fibroblast activation protein plays an important role in the promotion of tumor growth, and provides an attractive target for therapeutics designed to alter fibroblast activation protein-induced tumor growth by targeting its enzymatic activity.
  • [MeSH-major] Antigens, Neoplasm / physiology. Biomarkers, Tumor / physiology. Fibroblasts / metabolism. Neoplasms / enzymology. Serine Endopeptidases / physiology
  • [MeSH-minor] Alanine / chemistry. Animals. Antineoplastic Agents / pharmacology. Binding Sites. Blotting, Western. Catalytic Domain. Cell Line. Cell Line, Tumor. Cell Proliferation. DNA, Complementary / metabolism. Dipeptidyl-Peptidases and Tripeptidyl-Peptidases / metabolism. Flow Cytometry. Gelatinases. Humans. Hydrogen-Ion Concentration. Immunohistochemistry. Kinetics. Membrane Proteins. Mice. Microscopy, Fluorescence. Models, Molecular. Neoplasm Transplantation. Serine / chemistry. Time Factors. Transfection

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  • (PMID = 15767544.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09035-28; United States / NCI NIH HHS / CA / CA090468; United States / NCI NIH HHS / CA / CA103991-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / DNA, Complementary; 0 / Membrane Proteins; 452VLY9402 / Serine; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases; OF5P57N2ZX / Alanine
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58. Heynekamp JJ, Weber WM, Hunsaker LA, Gonzales AM, Orlando RA, Deck LM, Jagt DL: Substituted trans-stilbenes, including analogues of the natural product resveratrol, inhibit the human tumor necrosis factor alpha-induced activation of transcription factor nuclear factor kappaB. J Med Chem; 2006 Nov 30;49(24):7182-9
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  • [Title] Substituted trans-stilbenes, including analogues of the natural product resveratrol, inhibit the human tumor necrosis factor alpha-induced activation of transcription factor nuclear factor kappaB.
  • The transcription factor nuclear factor kappaB (NF-kappaB), which regulates expression of numerous antiinflammatory genes as well as genes that promote development of the prosurvival, antiapoptotic state is up-regulated in many cancer cells.
  • Resveratrol exhibits activity against a wide variety of cancer cells and has demonstrated activity as a cancer chemopreventive against all stages, i.e., initiation, promotion, and progression.
  • In the present study, phenolic analogues of resveratrol and a series of substituted trans-stilbenes without hydroxy groups were compared with resveratrol for their abilities to inhibit the human tumor necrosis factor alpha-induced (TNF-alpha) activation of NF-kappaB, using the Panomics NF-kappaB stable reporter cell line 293/NF-kappaB-luc.
  • The results from screening were confirmed using BV-2 microglial cells where resveratrol and analogues were shown to inhibit LPS-induced COX-2 expression.
  • [MeSH-major] Cyclooxygenase 2 Inhibitors / chemical synthesis. NF-kappa B / metabolism. Stilbenes / chemical synthesis. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Antioxidants / chemical synthesis. Antioxidants / chemistry. Antioxidants / pharmacology. Cell Line. Combinatorial Chemistry Techniques. Humans. Stereoisomerism. Structure-Activity Relationship

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  • (PMID = 17125270.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 0 / NF-kappa B; 0 / Stilbenes; 0 / Tumor Necrosis Factor-alpha; Q369O8926L / resveratrol
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59. Guan H, Williams JF, Ricciardi RP: Induction of neuronal and tumor-related genes by adenovirus type 12 E1A. J Virol; 2009 Jan;83(2):651-61
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  • [Title] Induction of neuronal and tumor-related genes by adenovirus type 12 E1A.
  • Substitution of a single amino acid in the spacer is able to abrogate Ad12 tumorigenesis.
  • To investigate the function of the spacer, microarray analysis was performed on cells transformed by tumorigenic and nontumorigenic Ad12s that differ only by one amino acid in the spacer.
  • Of these, more than half of the known genes with higher expression in the wild-type Ad12-transformed cells have neuronal-specific functions.
  • Some of the other differentially expressed genes are involved in the regulation of the cell cycle, transcription, cell structure, and tumor invasiveness.
  • Northern blot analyses of a subset of the neuronal genes, including Robo1, N-MYC, and alpha-internexin, confirmed their strong expression in multiple Ad12 tumorigenic cell lines.
  • In contrast, these neuronal genes displayed only minor or negligible expression in cells transformed by spacer-mutated Ad12.
  • Significantly, stable introduction of E1A-12 into nontumorigenic Ad5-transformed cells induced neuronal gene expression.
  • We found that the neuron-restrictive silencer factor, which serves as a master repressor of neuronal genes, was inactivated in both Ad12- and Ad5-transformed cells via cytoplasmic retention, though only Ad12-transformed cells exhibited neuronal gene induction.
  • Mutational analyses of the alpha-internexin promoter demonstrated that E1A-12-mediated neuronal gene induction further required the activation of neuronal promoter E-box elements.
  • These results indicate that the spacer is involved in mediating neuronal and tumor-related genes.

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  • (PMID = 18987153.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA029797; United States / NCI NIH HHS / CA / CA29797
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins
  • [Other-IDs] NLM/ PMC2612353
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60. Huang ST, Chen CT, Chieng KT, Huang SH, Chiang BH, Wang LF, Kuo HS, Lin CM: Inhibitory effects of a rice hull constituent on tumor necrosis factor alpha, prostaglandin E2, and cyclooxygenase-2 production in lipopolysaccharide-activated mouse macrophages. Ann N Y Acad Sci; 2005 May;1042:387-95
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  • [Title] Inhibitory effects of a rice hull constituent on tumor necrosis factor alpha, prostaglandin E2, and cyclooxygenase-2 production in lipopolysaccharide-activated mouse macrophages.
  • Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of alpha-tocopherol, a well-established antioxidant.
  • Isovitexin was able to reduce the amount of hydrogen peroxide production induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells.
  • In this study, we assessed its effects on the production of tumor necrosis factor alpha (TNF-alpha), prostaglandin E2 (PGE2), and the expression of cyclooxygenase-2 (COX-2) in LPS-activated RAW 264.7 macrophages.
  • Isovitexin inhibited the release of TNF-alpha, a proinflammatory cytokine, upon LPS activation with a 50% inhibitory concentration (IC50) of 78.6 microM.
  • [MeSH-major] Cyclooxygenase 2 / biosynthesis. Dinoprostone / biosynthesis. Lipopolysaccharides / pharmacology. Macrophages / drug effects. Macrophages / metabolism. Oryza / chemistry. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Apigenin / pharmacology. Cell Line. Mice

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  • (PMID = 15965085.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 38953-85-4 / isovitexin; 7V515PI7F6 / Apigenin; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
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61. Tellier E, Nègre-Salvayre A, Bocquet B, Itohara S, Hannun YA, Salvayre R, Augé N: Role for furin in tumor necrosis factor alpha-induced activation of the matrix metalloproteinase/sphingolipid mitogenic pathway. Mol Cell Biol; 2007 Apr;27(8):2997-3007
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  • [Title] Role for furin in tumor necrosis factor alpha-induced activation of the matrix metalloproteinase/sphingolipid mitogenic pathway.
  • Neutral sphingomyelinase (nSMase), the initial enzyme of the sphingolipid signaling pathway, is thought to play a key role in cellular responses to tumor necrosis factor alpha (TNF-alpha), such as inflammation, proliferation, and apoptosis.
  • The mechanism of TNF-alpha-induced nSMase activation is only partly understood.
  • Using biochemical, molecular, and pharmacological approaches, we found that nSMase activation triggered by TNF-alpha is required for TNF-alpha-induced proliferation and in turn requires a proteolytic cascade involving furin, membrane type 1 matrix metalloproteinase (MT1-MMP), and MMP2, and leading finally to extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and DNA synthesis, in smooth muscle cells (SMC) and fibroblasts.
  • Altogether these findings highlight a pivotal role for furin, MT1-MMP, and MMP2 in TNF-alpha-induced sphingolipid signaling, and they identify this system as a possible target to inhibit SMC proliferation in vascular diseases.
  • [MeSH-major] Furin / metabolism. Matrix Metalloproteinase 14 / metabolism. Matrix Metalloproteinase 2 / metabolism. Mitogens / metabolism. Sphingolipids / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Brefeldin A / pharmacology. Cell Proliferation / drug effects. Ceramides / metabolism. Enzyme Activation / drug effects. Fibroblasts / cytology. Fibroblasts / drug effects. Fibroblasts / enzymology. Humans. Lysophospholipids / metabolism. Mice. Models, Biological. Monensin / pharmacology. Myocytes, Smooth Muscle / drug effects. Myocytes, Smooth Muscle / enzymology. Rabbits. Signal Transduction / drug effects. Sphingomyelin Phosphodiesterase / metabolism. Sphingomyelins / metabolism. Sphingosine / analogs & derivatives. Sphingosine / metabolism. trans-Golgi Network / drug effects

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  • (PMID = 17283058.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Lysophospholipids; 0 / Mitogens; 0 / Sphingolipids; 0 / Sphingomyelins; 0 / Tumor Necrosis Factor-alpha; 20350-15-6 / Brefeldin A; 26993-30-6 / sphingosine 1-phosphate; 906O0YJ6ZP / Monensin; EC 3.1.4.12 / SMPD3 protein, human; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase; EC 3.4.21.75 / Furin; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.80 / Matrix Metalloproteinase 14; NGZ37HRE42 / Sphingosine
  • [Other-IDs] NLM/ PMC1899924
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62. Djouad F, Fritz V, Apparailly F, Louis-Plence P, Bony C, Sany J, Jorgensen C, Noël D: Reversal of the immunosuppressive properties of mesenchymal stem cells by tumor necrosis factor alpha in collagen-induced arthritis. Arthritis Rheum; 2005 May;52(5):1595-603
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  • [Title] Reversal of the immunosuppressive properties of mesenchymal stem cells by tumor necrosis factor alpha in collagen-induced arthritis.
  • OBJECTIVE: Adult mesenchymal stem cells (MSCs) represent promising tools for therapeutic applications such as tissue engineering and cellular therapy.
  • Recent data suggest that, due to their immunosuppressive nature, MSCs may be of interest to enhance allogeneic hematopoietic engraftment and prevent graft-versus-host disease.
  • Using a murine model of rheumatoid arthritis (RA), this study investigated whether the immunosuppressive properties of MSCs could be of therapeutic value to inhibit reactive T cells in autoimmune diseases such as RA.
  • The immunosuppressive properties of MSCs were determined in vitro in mixed lymphocyte reactions with or without the addition of tumor necrosis factor alpha (TNFalpha).
  • Using luciferase-expressing MSCs, we were unable to detect labeled cells in the articular environment of the knee, suggesting that worsening of the symptoms was unlikely due to the homing of MSCs in the joints.
  • Experiments in vitro showed that the addition of TNFalpha was sufficient to reverse the immunosuppressive effect of MSCs on T cell proliferation, and this observation was associated with an increase in interleukin-6 secretion.
  • [MeSH-major] Arthritis / therapy. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Collagen / administration & dosage. Immune Tolerance. Interleukin-10 / biosynthesis. Mesenchymal Stromal Cells / immunology. Mice. Mice, Inbred C3H

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  • (PMID = 15880818.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 9007-34-5 / Collagen
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63. Joachim RA, Sagach V, Quarcoo D, Dinh T, Arck PC, Klapp BF: Upregulation of tumor necrosis factor-alpha by stress and substance p in a murine model of allergic airway inflammation. Neuroimmunomodulation; 2006;13(1):43-50
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  • [Title] Upregulation of tumor necrosis factor-alpha by stress and substance p in a murine model of allergic airway inflammation.
  • Here, our aim was to investigate the influence of stress or exogenously applied SP on airway inflammation and on the local cytokine production of immune cells.
  • Cell numbers were determined in bronchoalveolar lavage (BAL) fluid.
  • Leukocytes from mediastinal lymph nodes were analyzed by flow cytometry to determine the percentages of T cells producing interleukin-4, interferon-gamma and tumor necrosis factor-alpha.
  • RESULTS: In BAL fluids of stressed or SP-treated animals, significantly higher total cell counts were found compared to non-stressed mice.
  • In lymph nodes, the percentage of TNF-alpha-positive T cells was higher in stressed mice and mice after application of SP.
  • In contrast, the influence of stress did not increase the percentages of interferon-gamma-positive CD3+ cells, meanwhile the application of SP increased the percentages of T cells positive for this cytokine.
  • CONCLUSION: Our data provide further evidence for a stress-mediating neuroimmunological pathway that, putatively via SP, is able to influence the composition of immune cells in different compartments of allergic airway inflammation.
  • [MeSH-major] Asthma / immunology. Lung / immunology. Stress, Physiological / complications. Stress, Physiological / immunology. Substance P / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Acoustic Stimulation / adverse effects. Animals. Antigens, CD3 / immunology. Disease Models, Animal. Interferon-gamma / immunology. Interferon-gamma / metabolism. Interleukin-4 / immunology. Interleukin-4 / metabolism. Lymph Nodes / immunology. Lymph Nodes / metabolism. Lymphocyte Count. Mice. Mice, Inbred BALB C. Neuroimmunomodulation / drug effects. Neuroimmunomodulation / immunology. Sound / adverse effects. T-Lymphocytes / drug effects. T-Lymphocytes / metabolism. Up-Regulation / drug effects. Up-Regulation / immunology

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  • (PMID = 16837794.001).
  • [ISSN] 1021-7401
  • [Journal-full-title] Neuroimmunomodulation
  • [ISO-abbreviation] Neuroimmunomodulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 33507-63-0 / Substance P; 82115-62-6 / Interferon-gamma
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64. Choi DE, Jeong JY, Lim BJ, Na KR, Shin YT, Lee KW: Pretreatment with the tumor nerosis factor-alpha blocker etanercept attenuated ischemia-reperfusion renal injury. Transplant Proc; 2009 Nov;41(9):3590-6
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  • [Title] Pretreatment with the tumor nerosis factor-alpha blocker etanercept attenuated ischemia-reperfusion renal injury.
  • INTRODUCTION: Tumor necrosis factor (TNF)-alpha mediates inflammation and apoptosis in ischemia-reperfusion (IR) injury of the kidneys.
  • Etanercept, a soluble TNF-alpha receptor, has shown anti-inflammatory and anti-apoptotic effects in several animal models of renal injury, including chronic insufficiency and unilateral ureteral obstruction.
  • Renal messenger RNA (mRNA) levels of TNF-alpha and monocyte chemotactic protein-1 (MCP-1) were measured by real-time polymerase chain reaction (PCR) at 24 hours after IR injury.
  • The protein levels of renal Bcl-2 associated X (Bax), B-cell lymphoma 2 (Bcl), extracellular signal-regulated kinase (ERK), and caspase-3 activation were evaluated using Western blot analysis.
  • The degree of apoptosis of renal tubular cells was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays.
  • Renal mRNA levels of TNF-alpha and MCP-1 in saline-treated IR rats were significantly higher than the levels in saline-treated sham rats, and TNF-alpha and MCP-1 mRNA levels in etanercept-treated IR rats were significantly lower than those in saline-treated IR rats.
  • Etanercept pretreatment of IR-injured rats significantly increased EKR phosphorylation and reduced the renal Bcl-2/Bax ratio, the renal caspase-3 activation, and the number of TUNEL-positive apoptotic cells.
  • [MeSH-major] Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Kidney / physiology. Receptors, Tumor Necrosis Factor / therapeutic use. Reperfusion Injury / prevention & control
  • [MeSH-minor] Animals. Blood Urea Nitrogen. Chemokine CCL2 / genetics. Creatinine / blood. Etanercept. Male. Polymerase Chain Reaction. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 19917350.001).
  • [ISSN] 1873-2623
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL2; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / RNA, Messenger; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; AYI8EX34EU / Creatinine; OP401G7OJC / Etanercept
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65. Matsuyoshi H, Hirata S, Yoshitake Y, Motomura Y, Fukuma D, Kurisaki A, Nakatsura T, Nishimura Y, Senju S: Therapeutic effect of alpha-galactosylceramide-loaded dendritic cells genetically engineered to express SLC/CCL21 along with tumor antigen against peritoneally disseminated tumor cells. Cancer Sci; 2005 Dec;96(12):889-96
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  • [Title] Therapeutic effect of alpha-galactosylceramide-loaded dendritic cells genetically engineered to express SLC/CCL21 along with tumor antigen against peritoneally disseminated tumor cells.
  • We tested a strategy to enhance the cross-talk between NKT cells and conventional antigen-specific T cells with the use of alpha GalCer-loaded dendritic cells genetically engineered to express antigen plus chemokine, attracting both conventional T cells and NKT cells.
  • DC genetically engineered to express a model antigen, OVA, along with SLC/CCL21 or monokine induced by IFN-gamma/CXCL9, had been generated using a method based on in vitro differentiation of DC from mouse ES cells.
  • The ES-DC were loaded with alpha-GalCer and transferred to mice bearing MO4, an OVA-expressing melanoma, and their capacity to evoke antitumor immunity was evaluated.
  • In vivo transfer of either OVA-expressing ES-DC, stimulating OVA-reactive T cells, or alpha-GalCer-loaded non-transfectant ES-DC, stimulating NKT cells, elicited a significant but limited degree of protection against the i.p. disseminated MO4.
  • A more potent antitumor effect was observed when alpha-GalCer was loaded to ES-DC expressing OVA before in vivo transfer, and the effect was abrogated by the administration of anti-CD8, anti-NK1.1 or anti-asialo GM1 antibody. alpha-GalCer-loaded double transfectant ES-DC expressing SLC along with OVA induced the most potent antitumor immunity.
  • Thus, alpha-GalCer-loaded ES-DC expressing tumor-associated antigen along with SLC can stimulate multiple subsets of effector cells to induce a potent therapeutic effect against peritoneally disseminated tumor cells.
  • The present study suggests a novel way to use alpha-GalCer in immunotherapy for peritoneally
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Chemokines, CC / genetics. Dendritic Cells / immunology. Galactosylceramides / therapeutic use. Neoplasms / immunology
  • [MeSH-minor] Animals. Antigens, Neoplasm / immunology. Cell Communication. Cell Line, Tumor. Cell Survival. Chemokine CCL21. Genetic Engineering. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Lymphocyte Activation / drug effects. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Ovalbumin / immunology. Recombinant Proteins. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

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  • [Copyright] (Cancer Sci 2005; 96: 889-896).
  • (PMID = 16367909.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Ccl21c protein, mouse; 0 / Chemokine CCL21; 0 / Chemokines, CC; 0 / Galactosylceramides; 0 / Recombinant Proteins; 0 / alpha-galactosylceramide; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 9006-59-1 / Ovalbumin
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66. Hosaka Y, Kirisawa R, Ueda H, Yamaguchi M, Takehana K: Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons. J Vet Med Sci; 2005 Oct;67(10):985-91
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  • [Title] Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons.
  • Tumor necrosis factor (TNF) receptors (TNF-R)-mediated cell survival or apoptosis has been demonstrated in many cells, but little is known about survival or apoptotic signals via TNF-R1 in tendinocytes.
  • Two distinct intracellular signaling pathways of TNFalpha, which lead to cell survival and apoptosis, might be present in tendinocytes mediated through TNF-R1.

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  • (PMID = 16276053.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / TNF Receptor-Associated Factor 2; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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67. Mohan S, Mohanasenthil, Paul SF, Shroff S, Venkatesan V: Interleukin-4-receptor alpha gene polymorphism and the risk of renal cell carcinoma in a South Indian population. Asian Pac J Cancer Prev; 2009 Apr-Jun;10(2):295-8
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  • [Title] Interleukin-4-receptor alpha gene polymorphism and the risk of renal cell carcinoma in a South Indian population.
  • The renal cell carcinoma (RCC) is a rare condition, accounting for only 3% of all adult malignancies although constituting 90% of kidney cancers.
  • The tumor is immunogenic and the host immune system may modulate the clinical course of the disease.
  • It has been reported that genetic polymorphisms in the interleukin-4-receptor alpha gene are associated with risk and prognosis in RCCs.
  • The present study is aimed at analyzing the presence and significance of the interleukin-4-receptor alpha Ile50Val and Gln576Arg polymorphisms in a group of RCC patients from South India.
  • A significant association was found between the IL4 R alpha Val/Val genotype and increased risk of RCC (OR: 3.45, CI: 1.15-10.38, P: 0.04).
  • Stratified analysis based on the genotypes and the stage of tumor revealed no significant association.
  • [MeSH-major] Carcinoma, Renal Cell / genetics. Kidney Neoplasms / genetics. Receptors, Interleukin-4 / genetics
  • [MeSH-minor] Adult. Aged. Alleles. Case-Control Studies. Female. Genetic Predisposition to Disease. Genotype. Humans. India / epidemiology. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. Polymorphism, Restriction Fragment Length. Prognosis. Risk

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  • (PMID = 19548368.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Receptors, Interleukin-4
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68. Akakura N, Hoogland C, Takada YK, Saegusa J, Ye X, Liu FT, Cheung AT, Takada Y: The COOH-terminal globular domain of fibrinogen gamma chain suppresses angiogenesis and tumor growth. Cancer Res; 2006 Oct 1;66(19):9691-7
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  • [Title] The COOH-terminal globular domain of fibrinogen gamma chain suppresses angiogenesis and tumor growth.
  • Fibrinogen is a major plasma protein (350 kDa) that induces proliferative signals by serving as a scaffold to support the binding of growth factors and to promote the cellular responses of adhesion, proliferation, and migration during wound healing, angiogenesis, and tumor growth.
  • The fibrinogen gamma chain has a COOH-terminal globular domain (gamma C, residues 151-411 of the gamma chain, 30 kDa) to which several integrin cell adhesion receptors (e.g., platelet alpha(IIb)beta(3), endothelial alpha(v)beta(3), and leukocyte alpha(M)beta(2)) bind.
  • We found that gamma C and its truncation mutant (designated gamma C399tr), with a deletion of the COOH-terminal 12 residues, induced apoptosis of endothelial cells and blocked tube formation of endothelial cells.
  • DLD-1 human colon cancer cells that secrete gamma C or gamma C399tr grew at similar levels in vitro but grew much slower in vivo than mock-transfected cells.
  • The recombinant purified gamma C399tr fragment markedly suppressed tumor growth, development of intratumoral vasculature, and tumor metastasis in vivo in the highly metastatic Met-1 breast cancer model.
  • The determinant responsible for binding to endothelial cells is cryptic in native fibrinogen but is exposed in gamma C and gamma C399tr.
  • These results suggest that fibrinogen has a novel cryptic determinant, which can exert apoptosis-inducing activity on endothelial cells when exposed, and polypeptides containing this determinant have therapeutic potential.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cells, Cultured / drug effects. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Colonic Neoplasms / secretion. Endothelial Cells / metabolism. Fibrin Fibrinogen Degradation Products / pharmacology. Humans. Integrin alphaVbeta3 / metabolism. Lung Neoplasms / blood supply. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mammary Neoplasms, Experimental / blood supply. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / secondary. Mice. Mice, Nude. Mice, SCID. Morphogenesis / drug effects. Mutation. Protein Binding. Protein Structure, Tertiary. Recombinant Fusion Proteins / physiology. Recombinant Fusion Proteins / secretion. Sequence Deletion. Transfection

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  • (PMID = 17018627.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA093373-04/10; United States / NCI NIH HHS / CA / CA113298; United States / NIGMS NIH HHS / GM / GM047157
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Fibrin Fibrinogen Degradation Products; 0 / Integrin alphaVbeta3; 0 / Peptide Fragments; 0 / Recombinant Fusion Proteins; 0 / fibrinogen D fragment; 0 / fibrinogen gamma (151-411); 0 / fibrinogen gamma 399 truncated; 9001-32-5 / Fibrinogen
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69. Lee HJ, Ji Y, Paul S, Maehr H, Uskokovic M, Suh N: Activation of bone morphogenetic protein signaling by a Gemini vitamin D3 analogue is mediated by Ras/protein kinase C alpha. Cancer Res; 2007 Dec 15;67(24):11840-7
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  • [Title] Activation of bone morphogenetic protein signaling by a Gemini vitamin D3 analogue is mediated by Ras/protein kinase C alpha.
  • We have previously shown that the novel Gemini vitamin D(3) analogue, Ro-438-3582 [Ro3582; 1 alpha,25-dihydroxy-20S,21(3-hydroxy-3-methylbutyl)-23-yne-26,27-hexafluorocholecalciferol], inhibited cell proliferation and activated the BMP/Smad signaling pathway in MCF10AT1 breast epithelial cells.
  • Among seven different serine/threonine kinase inhibitors that we tested, protein kinase C (PKC) inhibitors blocked the effects of Ro3582 on the phosphorylation of Smad1/5, mRNA synthesis for BMP-2 and BMP-6, and cell growth in MCF10AT1 cells.
  • Overexpression of PKC alpha, but not PKC epsilon, PKC delta or PKC zeta isoforms, increased Ro3582-induced phosphorylation of Smad1/5, suggesting that PKC alpha mediates the activation of Smad signaling and inhibition of cell proliferation.
  • Interestingly, the activation of Smad signaling by Ro3582 was shown in Ha-ras-transfected MCF10AT1 cells, but not in the parent cell line (MCF10A without Ras).
  • Inhibiting Ras activity blocked the translocation of PKC alpha to the plasma membrane and the phosphorylation of Smad1/5 induced by Ro3582, indicating that Ras is necessary for the activation of PKC alpha and Smad signaling.
  • In conclusion, Ro3582 inhibits cell proliferation and activates BMP/Smad signaling via a Ras and PKC alpha pathway in breast epithelial cells.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Calcitriol / analogs & derivatives. Calcitriol / pharmacology. Protein Kinase C-alpha / metabolism. ras Proteins / metabolism
  • [MeSH-minor] Breast / cytology. Breast / physiology. Breast Neoplasms. Carbazoles / pharmacology. Cell Line. Cell Line, Tumor. Epithelial Cells / cytology. Epithelial Cells / drug effects. Epithelial Cells / physiology. Female. Flavonoids / pharmacology. Humans. Indoles / pharmacology. Kinetics. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification

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  • (PMID = 18089814.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K22 CA 99990; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / R03 CA112642
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,25-dihydroxy-21-(3-hydroxy-3-methylbutyl)vitamin D(3); 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Bone Morphogenetic Proteins; 0 / Carbazoles; 0 / Flavonoids; 0 / Indoles; 0 / RNA, Neoplasm; 136194-77-9 / Go 6976; EC 2.7.11.13 / Protein Kinase C-alpha; EC 3.6.5.2 / ras Proteins; FXC9231JVH / Calcitriol
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70. Hohberger L, Wuertz BR, Xie H, Griffin T, Ondrey F: TNF-alpha drives matrix metalloproteinase-9 in squamous oral carcinogenesis. Laryngoscope; 2008 Aug;118(8):1395-9
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  • [Title] TNF-alpha drives matrix metalloproteinase-9 in squamous oral carcinogenesis.
  • We have previously demonstrated tumor necrosis factor (TNF)-alpha and its dependent cytokines are upregulated in saliva during oral carcinogenesis.
  • MATERIALS AND METHODS: In the present study, we examined NF-kappaB stimulation of matrix metalloproteinase (MMP)-9 in a precancerous keratinocyte cell line that models leukoplakia (Rhek cells).
  • We stimulated Rhek cells with both TNF-alpha and phorbol myristate acetate, known stimulants of NF-kappaB.
  • RESULTS: We discovered that the MMP-9 promoter was significantly stimulated by phorbol myristate acetate and TNF-alpha on luciferase reporter gene assays.
  • Functional activation of the MMP-9 protein was stimulated by TNF-alpha and PMA on a fluorescent enzyme-linked immunosorbent serologic assay.
  • CONCLUSIONS: We conclude the milieu cytokine, TNF-alpha, has the capacity to provide stimulation of events related to early invasion of oral cavity cancer, as judged by its ability to stimulate MMP-9.
  • [MeSH-major] Matrix Metalloproteinase 9 / metabolism. Mouth Neoplasms / metabolism. Neoplasm Invasiveness / physiopathology. Neoplasms, Squamous Cell / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Disease Progression. Enzyme Activation. Humans. Precancerous Conditions / metabolism. RNA, Messenger / metabolism. Saliva / metabolism. Tetradecanoylphorbol Acetate / metabolism. Tetradecanoylphorbol Acetate / pharmacology. Up-Regulation

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  • (PMID = 18496150.001).
  • [ISSN] 1531-4995
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / 1 R01 DE17734; United States / NCI NIH HHS / CA / P30 CA77598-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate
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71. del Fresno C, Otero K, Gómez-García L, González-León MC, Soler-Ranger L, Fuentes-Prior P, Escoll P, Baos R, Caveda L, García F, Arnalich F, López-Collazo E: Tumor cells deactivate human monocytes by up-regulating IL-1 receptor associated kinase-M expression via CD44 and TLR4. J Immunol; 2005 Mar 1;174(5):3032-40
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  • [Title] Tumor cells deactivate human monocytes by up-regulating IL-1 receptor associated kinase-M expression via CD44 and TLR4.
  • Although blood monocytes possess significant cytotoxic activity against tumor cells, tumor-infiltrating monocytes are commonly deactivated in cancer patients.
  • Monocytes pre-exposed to tumor cells show significantly decreased expression levels of TNF-alpha, IL-12p40, and IL-1R-associated kinase (IRAK)-1.
  • In this study, we show that IRAK-M expression is enhanced at the mRNA and protein level in human monocytes cultured in the presence of tumor cells.
  • IRAK-M was induced in monocytes upon coculturing with different tumor cells, as well as by fixed tumor cells and medium supplemented with the supernatant from tumor cell cultures.
  • Low concentrations of hyaluronan, a cell surface glycosaminoglycan released by tumor cells, also up-regulated IRAK-M.
  • The induction of IRAK-M by hyaluronan and tumor cells was abolished by incubation with anti-CD44 or anti-TLR4 blocking Abs.
  • Furthermore, down-regulation of IRAK-M expression by small interfering RNAs specific for IRAK-M reinstates both TNF-alpha mRNA expression and protein production in human monocytes re-exposed to a tumor cell line.
  • Altogether, our findings indicate that deactivation of human monocytes in the presence of tumor cells involves IRAK-M up-regulation, and this effect appears to be mediated by hyaluronan through the engagement of CD44 and TLR4.
  • [MeSH-major] Antigens, CD44 / physiology. Membrane Glycoproteins / physiology. Monocytes / immunology. Monocytes / metabolism. Protein Kinases / biosynthesis. Receptors, Cell Surface / physiology. Receptors, Interleukin-1 / biosynthesis. Up-Regulation / immunology
  • [MeSH-minor] Adult. Antibodies, Blocking / pharmacology. Cell Communication / immunology. Cell Line, Tumor. Coculture Techniques. Down-Regulation / immunology. Gene Expression Regulation, Neoplastic / immunology. HL-60 Cells. HeLa Cells. Humans. Hyaluronic Acid / pharmacology. Interleukin-1 Receptor-Associated Kinases. Jurkat Cells. Macrophage Activation / immunology. Male. Middle Aged. RNA, Messenger / antagonists & inhibitors. RNA, Messenger / biosynthesis. Toll-Like Receptor 4. Toll-Like Receptors. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 15728517.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antigens, CD44; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Interleukin-1; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha; 9004-61-9 / Hyaluronic Acid; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / IRAK3 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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72. Tomasetti M, Andera L, Alleva R, Borghi B, Neuzil J, Procopio A: Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis. FEBS Lett; 2006 Apr 3;580(8):1925-31
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  • [Title] Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis.
  • We evaluated the ability of alpha-tocopheryl succinate (alpha-TOS) to sensitise TRAIL-resistant malignant mesothelioma (MM) cells to TRAIL-induced apoptosis.
  • We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.
  • MM cells selected for TRAIL resistance expressed low cell surface levels of DR4 and DR5.
  • Treatment with sub-lethal doses of alpha-TOS restored expression of DR4 and DR5.
  • The ability of alpha-TOS to modulate expression of pro-apoptotic genes may play a role in sensitisation of tumour cells to immunological stimuli.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / pharmacology. Drug Resistance, Neoplasm / drug effects. Membrane Glycoproteins / pharmacology. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Protein p53 / metabolism. Vitamin E / analogs & derivatives
  • [MeSH-minor] Cytoplasm / metabolism. Humans. Neoplasms / metabolism. Neoplasms / pathology. Receptors, Cell Surface / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand. Recombinant Proteins / metabolism. TNF-Related Apoptosis-Inducing Ligand. Tocopherols. Tumor Cells, Cultured

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  • (PMID = 16529749.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols
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73. Jara JH, Singh BB, Floden AM, Combs CK: Tumor necrosis factor alpha stimulates NMDA receptor activity in mouse cortical neurons resulting in ERK-dependent death. J Neurochem; 2007 Mar;100(5):1407-20
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  • [Title] Tumor necrosis factor alpha stimulates NMDA receptor activity in mouse cortical neurons resulting in ERK-dependent death.
  • Previously, we demonstrated that glutamate and tumor necrosis factor alpha (TNFalpha) kill neurons via activation of the N-methyl-d-aspartate (NMDA) and TNFalpha receptors, respectively.
  • Stimulation of mouse cortical neuron cultures with TNFalpha results in a transient increase in NMDA receptor-dependent calcium influx that is additive with NMDA stimulation and inhibited by pre-treatment with the NMDA receptor antagonist, DL-2-amino-5-phosphonovaleric acid, or the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione.

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  • (PMID = 17241124.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE017102; United States / NIDCR NIH HHS / DE / R01 DE017102-03; United States / NCRR NIH HHS / RR / RR017699-077011; United States / NIA NIH HHS / AG / 1 R15 AG16192-01; United States / NIDCR NIH HHS / DE / R01 DE017102-01A1; United States / NIA NIH HHS / AG / 1 R03 AG20294-01; United States / NIDCR NIH HHS / DE / R01 DE017102-02; United States / NCRR NIH HHS / RR / P20 RR017699; United States / NCRR NIH HHS / RR / 1 P20 RR17699-01; United States / NCRR NIH HHS / RR / P20 RR017699-077011
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, N-Methyl-D-Aspartate; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tnfrsf1a protein, mouse; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS112596; NLM/ PMC3619402
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74. Sondarva G, Kundu CN, Mehrotra S, Mishra R, Rangasamy V, Sathyanarayana P, Ray RS, Rana B, Rana A: TRAF2-MLK3 interaction is essential for TNF-alpha-induced MLK3 activation. Cell Res; 2010 Jan;20(1):89-98
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  • [Title] TRAF2-MLK3 interaction is essential for TNF-alpha-induced MLK3 activation.
  • Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase that is activated by tumor necrosis factor-alpha (TNF-alpha) and specifically activates c-Jun N-terminal kinase (JNK) on TNF-alpha stimulation.
  • The mechanism by which TNF-alpha activates MLK3 is still not known.
  • Endogenous TRAF2 and MLK3 associate with each other in response to TNF-alpha treatment in a time-dependent manner.
  • The association between MLK3 and TRAF2 mediates MLK3 activation and competition with the TRAF2 deletion mutant that binds to MLK3 attenuates MLK3 kinase activity in a dose-dependent manner, on TNF-alpha treatment.
  • Furthermore the downstream target of MLK3, JNK was activated by TNF-alpha in a TRAF2-dependent manner.
  • Hence, our data show that the direct interaction between TRAF2 and MLK3 is required for TNF-alpha-induced activation of MLK3 and its downstream target, JNK.

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  • (PMID = 19918265.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM055835-07A3; United States / NCI NIH HHS / CA / R21 CA121221; United States / NIGMS NIH HHS / GM / GM55835; United States / NCI NIH HHS / CA / CA121221; United States / NIGMS NIH HHS / GM / R01 GM055835-07A3; United States / NIGMS NIH HHS / GM / R01 GM055835
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TNF Receptor-Associated Factor 2; 0 / TNF Receptor-Associated Factor 5; 0 / TNF Receptor-Associated Factor 6; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / mitogen-activated protein kinase kinase kinase 11
  • [Other-IDs] NLM/ NIHMS149286; NLM/ PMC2801772
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75. Zannetti A, Del Vecchio S, Iommelli F, Del Gatto A, De Luca S, Zaccaro L, Papaccioli A, Sommella J, Panico M, Speranza A, Grieco P, Novellino E, Saviano M, Pedone C, Salvatore M: Imaging of alpha(v)beta(3) expression by a bifunctional chimeric RGD peptide not cross-reacting with alpha(v)beta(5). Clin Cancer Res; 2009 Aug 15;15(16):5224-33
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  • [Title] Imaging of alpha(v)beta(3) expression by a bifunctional chimeric RGD peptide not cross-reacting with alpha(v)beta(5).
  • PURPOSE: To test whether a novel bifunctional chimeric peptide comprising a cyclic Arg-Gly-Asp pentapeptide covalently bound to an echistatin domain can discriminate alpha(v)beta(3) from alpha(v)beta(5) integrin, thus allowing the in vivo selective visualization of alpha(v)beta(3) expression by single-photon and positron emission tomography (PET) imaging.
  • EXPERIMENTAL DESIGN: The chimeric peptide was preliminarily tested for inhibition of alpha(v)beta(3)-dependent cell adhesion and competition of 125I-echistatin binding to membrane of stably transfected K562 cells expressing alpha(v)beta(3) (Kalpha(v)beta(3)) or alpha(v)beta(5) (Kalpha(v)beta(5)) integrin.
  • Nude mice bearing tumors from Kalpha(v)beta(3), Kalpha(v)beta(5), U87MG human glioblastoma, and A431 human epidermoid cells were subjected to single-photon and PET imaging.
  • RESULTS: Adhesion and competitive binding assays showed that the novel chimeric peptide selectively binds to alpha(v)beta(3) integrin and does not cross-react with alpha(v)beta(5).
  • In agreement with in vitro findings, single-photon and PET imaging studies showed that the radiolabeled chimeric peptide selectively localizes in tumor xenografts expressing alphavbeta3 and fails to accumulate in those expressing alpha(v)beta(5) integrin.
  • When 18F-labeled truncated derivative was used for PET imaging, alphavbeta3- and alpha(v)beta(5)-expressing tumors were visualized, indicating that the five C-terminal amino acids are required to differentially bind the two integrins.
  • [MeSH-minor] Amino Acid Sequence. Animals. Humans. Iodine Radioisotopes / metabolism. K562 Cells. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Peptides / chemistry. Peptides / metabolism. Protein Binding. Recombinant Fusion Proteins / metabolism. Substrate Specificity. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 19671851.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 0 / Iodine Radioisotopes; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, Vitronectin; 0 / Recombinant Fusion Proteins; 0 / integrin alphaVbeta5; 118337-11-4 / echistatin; 99896-85-2 / arginyl-glycyl-aspartic acid
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76. Yoshioka Y, Watanabe H, Morishige T, Yao X, Ikemizu S, Nagao C, Ahmad S, Mizuguchi K, Tsunoda S, Tsutsumi Y, Mukai Y, Okada N, Nakagawa S: Creation of lysine-deficient mutant lymphotoxin-alpha with receptor selectivity by using a phage display system. Biomaterials; 2010 Mar;31(7):1935-43
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  • [Title] Creation of lysine-deficient mutant lymphotoxin-alpha with receptor selectivity by using a phage display system.
  • The cytokine lymphotoxin-alpha (LT alpha) activates various biological functions through its three receptor subtypes, tumor necrosis factor receptor 1 (TNFR1), TNFR2 and herpes virus entry mediator (HVEM), but the relative contribution of each receptor to each function is unclear.
  • Therefore it is important to create mutant LT alpha with receptor selectivity for optimized cancer therapy and the analysis of receptor function.
  • Here, we attempted to create a lysine-deficient mutant LT alpha with TNFR1-selective bioactivity using a phage display technique.
  • We obtained the TNFR1-selective mutant LT alpha R1selLT, which contained the mutations K19N, K28Q, K39S, K84Q, K89V, and K119H.
  • Compared with wild-type LT alpha (wtLT alpha), R1selLT showed several-fold higher bioactivity via TNFR1 but 40-fold lower bioactivity via TNFR2.
  • Kinetic association-dissociation parameters of R1selLT with TNFR2 were higher than those of wtLT alpha, whereas these parameters of R1selLT with TNFR1 were lower than those of wtLT alpha, suggesting that destabilization of the R1selLT-TNFR2 complex causes the decreased bioactivity of R1selLT on TNFR2.
  • R1selLT likely will be useful in cancer therapy and in analysis of the LT alpha structure-function relationship.
  • [MeSH-major] Lymphotoxin-alpha / metabolism. Lysine / deficiency. Mutant Proteins / metabolism. Peptide Library. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Death. Cell Line, Tumor. Humans. Isoelectric Point. Kinetics. Mice. Models, Molecular. Molecular Sequence Data. Point Mutation / genetics. Protein Binding

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  • [Copyright] (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19853911.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lymphotoxin-alpha; 0 / Mutant Proteins; 0 / Peptide Library; 0 / Receptors, Cell Surface; K3Z4F929H6 / Lysine
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77. El Hage F, Vergnon I, Grunenwald D, Soria JC, Chouaib S, Mami-Chouaib F: Generation of diverse mutated tumor antigen-specific cytotoxic T lymphocytes in a lung cancer patient with long survival. Oncol Rep; 2005 Sep;14(3):763-9
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  • [Title] Generation of diverse mutated tumor antigen-specific cytotoxic T lymphocytes in a lung cancer patient with long survival.
  • We have identified an antigen recognized on a large cell carcinoma of the lung by tumor-specific cytotoxic T lymphocytes (CTL).
  • The antigenic peptide is encoded by a mutated alpha-actinin-4 gene and presented by human leukocyte antigen (HLA)-A2.
  • Using HLA-A2-peptide tetramers, we have derived from patient peripheral blood lymphocytes (PBL) and autologous tumor infiltrating lymphocytes (TIL) several mutated alpha-actinin-4-specific T cell clones.
  • These clones displayed similar tetramer staining but distinct T cell receptor (TCR) usage and antitumor reactivity.
  • Indeed, TIL clones lysed more efficiently the autologous tumor cells and released higher cytokine levels than PBL clones.
  • Importantly, treatment of cancer cells with interferon-gamma enhanced their susceptibility to PBL clone-mediated lysis correlated with increase in HLA-class I expression.
  • The present findings provide evidence that an immune T cell response took place in a lung cancer patient with favorable clinical evolution and suggest that CTL, recognizing a truly tumor-specific antigen, may contribute to controlling the tumor.
  • [MeSH-major] Actinin / genetics. Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology. Microfilament Proteins / genetics. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 16077989.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / HLA-A2 Antigen; 0 / Microfilament Proteins; 11003-00-2 / Actinin
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78. Kobayashi M, Suzuki K, Yashi M, Yuzawa M, Takayashiki N, Morita T: Tumor infiltrating dendritic cells predict treatment response to immmunotherapy in patients with metastatic renal cell carcinoma. Anticancer Res; 2007 Mar-Apr;27(2):1137-41
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  • [Title] Tumor infiltrating dendritic cells predict treatment response to immmunotherapy in patients with metastatic renal cell carcinoma.
  • BACKGROUND: Although renal cell carcinoma (RCC) is considered to be an immunogenic tumor, the role of immunogenicity in this tumor for predicting treatment response has been little investigated.
  • PATIENTS AND METHODS: Resected RCC specimens from 25 patients who received cytokine treatment for metastases were investigated using immunohistochemistry for CD83+ or S100+ dendritic cells (DCs), CD8+ T-cells, HLA-DR+ tumor cells, CD68+ tumor associated macrophages, microvascular density and vascular endotherial growth factor.
  • RESULTS: Among the examined parameters, DCs status showed predictive value, that is, higher numbers of CD83+ or S100+ cells in tumors were associated with favorable treatment response.
  • CONCLUSION: Increased tumor infiltration of mature DCs would be a predictor of treatment response and outcome in metastatic RCC patients, who receive immunotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Renal Cell / immunology. Carcinoma, Renal Cell / therapy. Dendritic Cells / immunology. Immunotherapy / methods. Interferon-alpha / therapeutic use. Kidney Neoplasms / immunology. Kidney Neoplasms / therapy

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  • (PMID = 17465253.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD83 antigen; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Interferon-alpha; 0 / Interleukin-2; 0 / Membrane Glycoproteins; 0 / Pyrimidines; 0 / Vascular Endothelial Growth Factor A
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79. Jeon ES, Heo SC, Lee IH, Choi YJ, Park JH, Choi KU, Park DY, Suh DS, Yoon MS, Kim JH: Ovarian cancer-derived lysophosphatidic acid stimulates secretion of VEGF and stromal cell-derived factor-1 alpha from human mesenchymal stem cells. Exp Mol Med; 2010 Apr 30;42(4):280-93
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  • [Title] Ovarian cancer-derived lysophosphatidic acid stimulates secretion of VEGF and stromal cell-derived factor-1 alpha from human mesenchymal stem cells.
  • Lysophosphatidic acid (LPA) stimulates growth and invasion of ovarian cancer cells and tumor angiogenesis.
  • Cancer-derived LPA induces differentiation of human adipose tissue-derived mesenchymal stem cells (hASCs) to alpha-smooth muscle actin (alpha-SMA)-positive cancer-associated fibroblasts.
  • Conditioned medium (CM) from the OVCAR-3 and SKOV3 ovarian cancer cell lines stimulated secretion angiogenic factors such as stromal-derived factor-1 alpha (SDF-1 alpha) and VEGF from hASCs.
  • Pretreatment with the LPA receptor inhibitor Ki16425 or short hairpin RNA lentiviral silencing of the LPA((1)) receptor abrogated the cancer CM-stimulated expression of alpha-SMA, SDF-1, and VEGF from hASCs.
  • LPA induced expression of myocardin and myocardin-related transcription factor-A, transcription factors involved in smooth muscle differentiation, in hASCs. siRNA-mediated depletion of endogenous myocardin and MRTF-A abrogated the expression of alpha-SMA, but not SDF-1 and VEGF.
  • LPA activated RhoA in hASCs and pretreatment with the Rho kinase inhibitor Y27632 completely abrogated the LPA-induced expression of alpha-SMA, SDF-1, and VEGF in hASCs.
  • Moreover, LPA-induced alpha-SMA expression was abrogated by treatment with the ERK inhibitor U0126 or the phosphoinositide-3-kinase inhibitor LY294002, but not the PLC inhibitor U73122.
  • [MeSH-major] Chemokine CXCL12 / secretion. Lysophospholipids / pharmacology. Mesenchymal Stromal Cells / drug effects. Mesenchymal Stromal Cells / secretion. Ovarian Neoplasms / metabolism. Vascular Endothelial Growth Factors / secretion
  • [MeSH-minor] Actins / metabolism. Adipose Tissue / cytology. Cell Line, Tumor. Culture Media, Conditioned. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Female. Humans. Microphthalmia-Associated Transcription Factor / metabolism. Neovascularization, Physiologic / drug effects. Paracrine Communication / drug effects. Receptors, Lysophosphatidic Acid / metabolism. Signal Transduction / drug effects. rho-Associated Kinases / metabolism. rhoA GTP-Binding Protein / metabolism