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[Title] Absence of hotspot mutations in exons 9 and 20 of the PIK3CA gene in human oral squamous cell carcinoma in the Greek population.

Recent studies have reported high frequencies of somatic hotspot mutations in the phosphatidylinositol-3 kinase catalytic alpha (PIK3CA) gene, which encodes for one of these kinases, in several human solid tumors, including oral squamous cell carcinoma (OSCC).

STUDY DESIGN: Eighty-six formalin-fixed and paraffin-embedded primary tumor specimens were analyzed by direct genomic DNA sequencing.

RESULTS: No hotspot mutations were detected in any of the samples.

[MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Squamous Cell / enzymology. Exons / genetics. Mouth Neoplasms / enzymology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Cytosine. Female. Gingival Neoplasms / enzymology. Gingival Neoplasms / genetics. Greece. Guanine. Humans. Introns / genetics. Male. Mandibular Neoplasms / enzymology. Mandibular Neoplasms / genetics. Middle Aged. Mouth Mucosa / pathology. Neoplasm Staging. Polymerase Chain Reaction. Polymorphism, Genetic / genetics. Sequence Analysis, DNA. Thymine. Tongue Neoplasms / enzymology. Tongue Neoplasms / genetics. Young Adult

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[Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.

(PMID = 20416519.001).

[ISSN] 1528-395X

[Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics

[ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 5Z93L87A1R / Guanine; 8J337D1HZY / Cytosine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; QR26YLT7LT / Thymine

   

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[Title] Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha.

Acute promyelocytic leukemia (APL) is invariably associated with chromosomal translocation to retinoic acid receptor alpha (RARalpha) locus.

It was thought that the fusion protein PML-RARalpha acts as a double dominant negative mutant to inhibit the PML and RARalpha signaling.

In an attempt to study the physiological role of retinoic acid in mammary gland development, we created a transgenic model system expressing a dominant negative RARalpha under the regulation of murine mammary tumor viral promoter.

Retinoic acid blocked tumor development ex vivo through induction of apoptosis.

Thus, our results suggested that disruption of RARalpha signaling was the first essential step in the development of APL in vivo.

[MeSH-major] Gene Expression Regulation / physiology. Genes, Dominant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Receptors, Retinoic Acid / genetics

[MeSH-minor] Acute Disease. Animals. Apoptosis. Cell Proliferation. Female. Humans. Male. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Survival Rate. Tretinoin / pharmacology. Tumor Cells, Cultured

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(PMID = 16273555.001).

[ISSN] 0899-1987

[Journal-full-title] Molecular carcinogenesis

[ISO-abbreviation] Mol. Carcinog.

[Language] eng

[Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA89526

[Publication-type] Comparative Study; 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 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin

   

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[Title] Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer.

Recently we have identified a new type of cancer cell called precancerous stem cells (pCSCs) and proposed that cancer may arise from a lengthy development process of tumor initiating cells (TICs) --> pCSCs --> cancer stem cells (CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer cells), accompanied by clonal evolutionary epigenetic and genetic alterations.

In this study, we investigated whether aberrant DNA methylation can be used as a biomarker for the differentiation between premalignant and malignant lesions in the colorectum.

The profile of global DNA and estrogen receptor (ER)-alpha gene methylation during cancer development was determined by analysis of 5-methylcytosine (5-MeC) using immunohistochemical (IHC) staining, dot blot analysis or a quantitative gene methylation assay (QGMA).

Herein we show that global DNA hypomethylation and ER-alpha gene hypermethylation are progressively enhanced from hyperplastic polyps (HPs) --> adenomatous polyps (APs) --> adenomatous carcinoma (AdCa).

In normal colorectal mucosa, while global DNA methylation was not affected by aging, ER-alpha gene methylation was significantly increased with aging.

Taken together, reversibility of aberrant global DNA and ER-alpha gene methylation distinguishes colorectal precancer from cancer.

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(PMID = 18830381.001).

[ISSN] 1936-2625

[Journal-full-title] International journal of clinical and experimental pathology

[ISO-abbreviation] Int J Clin Exp Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Keywords] NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation

   

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[Title] Roles of peroxisome proliferator-activated receptor-alpha and -gamma in the development of non-small cell lung cancer.

Peroxisome proliferator-activated receptor (PPAR)-α and PPARγ participate in cell proliferation and apoptosis.

The roles of PPARα and -γ were investigated in the development of pulmonary tumors induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)-lbutanone (NNK).

Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung tumor tissues.

Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung tumors.

Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung tumors induced by NNK.

Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis.

The results suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung tumors, as well as accelerate the therapy of lung cancer.

Our findings may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα as tumor markers for lung cancer.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. PPAR alpha / metabolism. PPAR gamma / metabolism. Precancerous Conditions / pathology

[MeSH-minor] Animals. Disease Progression. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hydroxyeicosatetraenoic Acids / metabolism. Ligands. Linoleic Acids / metabolism. Lipid Metabolism / drug effects. Lipid Metabolism / genetics. Male. Mice. Nitrosamines. Retinoid X Receptor alpha / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Thiazolidinediones / pharmacology. Transcription, Genetic / drug effects

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(PMID = 20081051.001).

[ISSN] 1535-4989

[Journal-full-title] American journal of respiratory cell and molecular biology

[ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Hydroxyeicosatetraenoic Acids; 0 / Ligands; 0 / Linoleic Acids; 0 / Nitrosamines; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Retinoid X Receptor alpha; 0 / Thiazolidinediones; 5204-88-6 / 13-hydroxy-9,11-octadecadienoic acid; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 73945-47-8 / 15-hydroxy-5,8,11,13-eicosatetraenoic acid; X4OV71U42S / pioglitazone

   

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[Title] ICAM-1 contributes to but is not essential for tumor antigen cross-priming and CD8+ T cell-mediated tumor rejection in vivo.

ICAM-1 has been described to provide both adhesion and costimulatory functions during T cell activation.

In the setting of antitumor immunity, ICAM-1/LFA-1 interactions could be important at the level of T cell priming by APCs in draining lymph nodes as well as for transendothelial migration and tumor cell recognition at the tumor site.

To determine the contribution of ICAM-1 to tumor rejection in vivo, we performed adoptive transfer of 2C TCR-transgenic/RAG2(-/-) T cells into TCRalpha(-/-) vs ICAM(-/-)/TCRalpha(-/-) recipient animals.

ICAM-1-deficient mice successfully rejected HTR.C tumors expressing Ld recognized by the 2C TCR, albeit with a kinetic delay.

Inasmuch as HTR.C tumor cells themselves express ICAM-1, a second model was pursued using B16-F10 melanoma cells that lack ICAM-1 expression.

These cells were transduced to express the SIYRYYGL peptide recognized by the 2C TCR in the context of Kb, which is cross-presented by APCs in H-2b mice in vivo.

These tumors also grew more slowly but were eventually rejected by the majority of ICAM-1(-/-)/TCRalpha(-/-) recipients.

Delayed rejection in ICAM-1(-/-) mice was associated with diminished T cell priming as assessed by ELISPOT.

In contrast, T cell penetration into the tumor was comparable in wild-type and ICAM-1(-/-) hosts, and adoptively transferred primed effector 2C cells rejected normally in ICAM-1(-/-) recipients.

Our results suggest that ICAM-1 contributes to but is not absolutely required for CD8+ T cell-mediated tumor rejection in vivo and dominantly acts at the level of priming rather than the effector phase of the antitumor immune response.

[MeSH-major] Antigens, Neoplasm. CD8-Positive T-Lymphocytes / immunology. Intercellular Adhesion Molecule-1 / immunology

[MeSH-minor] Adoptive Transfer. Animals. Antigen Presentation. Cell Line, Tumor. In Vitro Techniques. Mice. Mice, Knockout. Mice, Transgenic. Neoplasm Transplantation. Neoplasms, Experimental / immunology. Receptors, Antigen, T-Cell, alpha-beta / deficiency. Receptors, Antigen, T-Cell, alpha-beta / genetics

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(PMID = 15749875.001).

[ISSN] 0022-1767

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / 5 T32 GM07281; United States / NCI NIH HHS / CA / P01CA97296

[Publication-type] Journal Article; 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 / Receptors, Antigen, T-Cell, alpha-beta; 126547-89-5 / Intercellular Adhesion Molecule-1

   

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[Title] Inhibition of HIF-1 alpha and VEGF expression by the chemopreventive bioflavonoid apigenin is accompanied by Akt inhibition in human prostate carcinoma PC3-M cells.

Progression of cancer leads to hypoxic solid tumors that mount specific cell signaling responses to low oxygen conditions.

An important objective of anti-cancer therapy is the development of new drugs that suppress hypoxic responses in solid tumors.

Apigenin is a natural flavone that has been shown to have chemopreventive and/or anti-cancer properties against a number of tumor types.

In this study, we have investigated the effects of apigenin on expression of hypoxia-inducible factor-1 (HIF-1) in human metastatic prostate PC3-M cancer cells.

We found that hypoxia induced a time-dependent increase in the level of HIF-1alpha subunit protein in PC3-M cells, and treatment with apigenin markedly decreased HIF-1alpha expression under both normoxic and hypoxic conditions.

Further, apigenin prevented the activation of the HIF-1 downstream target gene vascular endothelial growth factor (VEGF).

We also found that apigenin inhibited Akt and GSK-3beta phosphorylation in PC3-M cells.

Taken together, our results identify apigenin as a bioflavonoid that inhibits hypoxia-activated pathways linked to cancer progression in human prostate cancer, in particular the PI3K/Akt/GSK-3 pathway.

Further studies on the mechanism of action of apigenin will likely provide new insight into its applicability for pharmacologic targeting of HIF-1alpha for cancer therapeutic or chemopreventive purposes.

[MeSH-major] Apigenin / pharmacology. Flavonoids / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Prostatic Neoplasms / pathology. Vascular Endothelial Growth Factor A / genetics

[MeSH-minor] Cell Hypoxia. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Neoplasm Metastasis

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(PMID = 18240292.001).

[ISSN] 1098-2744

[Journal-full-title] Molecular carcinogenesis

[ISO-abbreviation] Mol. Carcinog.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P50 CA90386; United States / PHS HHS / / T32-0700085

[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 / Flavonoids; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 7V515PI7F6 / Apigenin

   

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[Title] Selective tumor cell targeting using low-affinity, multivalent interactions.

This report highlights the advantages of low-affinity, multivalent interactions to recognize one cell type over another.

Our goal was to devise a strategy to mediate selective killing of tumor cells, which are often distinguished from normal cells by their higher levels of particular cell surface receptors.

To test whether multivalent interactions could lead to highly specific cell targeting, we used a chemically synthesized small-molecule ligand composed of two distinct motifs:.

(1) an Arg-Gly-Asp (RGD) peptidomimetic that binds tightly (Kd approximately 10(-9)M) to alphavbeta3 integrins and (2) the galactosyl-alpha(1-3)galactose (alpha-Gal epitope), which is recognized by human anti-alpha-galactosyl antibodies (anti-Gal).

Importantly, anti-Gal binding requires a multivalent presentation of carbohydrate residues; anti-Gal antibodies interact weakly with the monovalent oligosaccharide (Kd approximately 10(-5)M) but bind tightly (Kd approximately 10(-11) M) to multivalent displays of alpha-Gal epitopes.

Such a display is generated when the bifunctional conjugate decorates a cell possessing a high level of alphavbeta3 integrin; the resulting cell surface, which presents many alpha-Gal epitopes, can recruit anti-Gal, thereby triggering complement-mediated lysis.

Only those cells with high levels of the integrin receptor are killed.

In contrast, doxorubicin tethered to the RGD-based ligand affords indiscriminate cell death.

These results highlight the advantages of exploiting the type of the multivalent recognition processes used by physiological systems to discriminate between cells.

Our results have implications for the treatment of cancer and other diseases characterized by the presence of deleterious cells.

[MeSH-major] Antineoplastic Agents / chemical synthesis. Disaccharides / metabolism. Neoplasms / drug therapy. Oligopeptides / metabolism

[MeSH-minor] Cell Line, Tumor. Complement System Proteins / physiology. Doxorubicin / pharmacology. Drug Design. Humans. Integrin alphaVbeta3 / analysis. Integrin alphaVbeta3 / metabolism. Molecular Weight

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(PMID = 17291050.001).

[ISSN] 1554-8937

[Journal-full-title] ACS chemical biology

[ISO-abbreviation] ACS Chem. Biol.

[Language] eng

[Grant] United States / NIAID NIH HHS / AI / AI55258; United States / NCI NIH HHS / CA / CA14520; United States / NIGMS NIH HHS / GM / GM07215

[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 / Antineoplastic Agents; 0 / Disaccharides; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 13168-24-6 / galactosyl-(1-3)galactose; 80168379AG / Doxorubicin; 9007-36-7 / Complement System Proteins; 99896-85-2 / arginyl-glycyl-aspartic acid

   

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[Title] Severe malaria in Cameroonian children: correlation between plasma levels of three soluble inducible adhesion molecules and TNF-alpha.

Plasma levels of three soluble inducible adhesion molecules, namely: intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1) and endothelial leucocyte adhesion molecule-1 (sELAM-1) or sE-selectin and the pro-inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha) were measured in well-defined clinical groups of children with severe and uncomplicated malaria.

Results showed significantly increased plasma concentrations of sICAM-1, sVCAM-1 and sE-selectin in children with severe malaria compared to those with uncomplicated malaria and healthy children (P<0.001).

TNF-alpha levels increased significantly in children with severe malaria, approximately 2-folds compared to those with uncomplicated malaria and about 3-folds compared to healthy children (P<0.001).

More importantly, levels of TNF-alpha strongly correlated with those of the three adhesion molecules and were significantly associated with increased risk of death (P=0.03).

In addition, children who died from severe malaria showed higher mean levels of all measured factors compared to those who recovered, with significant differences observed with sICAM-1 (P<0.001) and sE-selectin (P=0.002).

Taken together, these results confirm the role of TNF-alpha and the three adhesion molecules in pathogenic processes associated with severe malaria in children, and suggest an association between sICAM-1 and severe malarial anemia.

[MeSH-major] Cell Adhesion Molecules / blood. Malaria, Falciparum / immunology. Malaria, Falciparum / physiopathology. Plasmodium falciparum / pathogenicity. Severity of Illness Index. Tumor Necrosis Factor-alpha / blood

[MeSH-minor] Animals. Cameroon / epidemiology. Child. Child, Preschool. E-Selectin / blood. Female. Humans. Infant. Intercellular Adhesion Molecule-1 / blood. Malaria, Cerebral / epidemiology. Malaria, Cerebral / immunology. Malaria, Cerebral / parasitology. Malaria, Cerebral / physiopathology. Male. Solubility. Up-Regulation. Vascular Cell Adhesion Molecule-1 / blood

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(PMID = 17397790.001).

[ISSN] 0001-706X

[Journal-full-title] Acta tropica

[ISO-abbreviation] Acta Trop.

[Language] eng

[Grant] United States / FIC NIH HHS / TW / 5D43 TW01264

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / E-Selectin; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1

   

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[Title] Interferon-alpha and viral triggers promote functional maturation of human monocyte-derived dendritic cells.

BACKGROUND: Type I interferons (IFNs) play an important role in the pathogenesis of many autoimmune disorders including psoriasis.

In the presence of IFN-alpha and granulocyte/macrophage colony-stimulating factor (GM-CSF), monocytes differentiate into dendritic cells (DCs) referred to as IFN-DCs.

OBJECTIVES: Recently, it was shown that single-stranded RNA (ssRNA) triggers TLR7 and TLR8; therefore we studied ssRNA, as a surrogate for ssRNA viruses and their impact on IFN-DCs.

METHODS: We established culture conditions for IFN-DCs, generated from plastic adherent monocytes using GM-CSF plus IFN-alpha.

The ability of IFN-DCs to stimulate allogeneic T-cell proliferation was evaluated in a mixed leucocyte reaction.

RESULTS: We found that IFN-DCs express mRNA for TLR7 and TLR8 and that ssRNA stimulation significantly improves their costimulatory molecule expression, stabilizes their phenotype and enhances their capacity to stimulate naive T-cell proliferation.

In contrast, ssRNA stimulation led to a significant production of IL-12p70, IL-1beta, IL-6 and tumour necrosis factor alpha.

CONCLUSIONS: Our study sheds light on a potential role for IFN-alpha and viral infections in triggering DC populations in psoriasis.

These results provide additional data for the better understanding of human autoimmune and antiviral responses and may also have implications for strategies developing cancer immunotherapy.

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(PMID = 18371115.001).

[ISSN] 0007-0963

[Journal-full-title] The British journal of dermatology

[ISO-abbreviation] Br. J. Dermatol.

[Language] ENG

[Grant] United States / NIAMS NIH HHS / AR / AR040065-17; United States / NIAMS NIH HHS / AR / R01 AR040065-17

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cytokines; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

[Other-IDs] NLM/ NIHMS152059; NLM/ PMC2829135

   

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[Title] Tumor necrosis factor alpha inhibitors for the treatment of dermatologic diseases.

Tumor necrosis factor alpha (TNFalpha) is involved in cell differentiation, mitogenesis, cytotoxic responses, inflammation, immunomodulation, and wound healing.

Because of its numerous roles, it was thought that inhibition of TNF may aid in the treatment of certain dermatologic diseases such as psoriasis, hidradentitis suppurativa, pyoderma gangrenosum, Behcet 's syndrome, and graft versus host disease.

The efficacy of these agents has proven impressive and short-term side effects have been few and relatively benign.

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(PMID = 15916184.001).

[ISSN] 1060-3441

[Journal-full-title] Dermatology nursing

[ISO-abbreviation] Dermatol Nurs

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Dermatologic Agents; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept

[Number-of-references] 57

   

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[Title] Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells.

Nicotinic acetylcholine receptors (nAChR) are expressed on non-neuronal cell types, including normal bronchial epithelial cells, and nicotine has been reported to cause Akt activation in cultured normal airway cells.

This study documents mRNA and protein expression of subunits known to form a muscle-type nAChR in non-small cell lung cancer (NSCLC) cell lines.

In one NSCLC examined, mRNA and protein for a heteropentamer neuronal-type alpha3beta2 nAChR was detected in addition to a muscle-type receptor.

Protein for the alpha5 nAChR was also detected in NSCLC cells.

Although, mRNA for the alpha7 nAChR subunit was observed in all cell lines, alpha7 protein was not detectable by immunoblot in NSCLC cell extracts.

Immunohistochemistry (IHC) of NSCLC primary tissues from 18 patients demonstrated protein expression of nAChR alpha1 and beta1 subunits, but not alpha7 subunit, in lung tumors, indicating preferential expression of the muscle-type receptor.

In addition, the beta1 subunit showed significantly increased expression in lung tumors as compared to non-tumor bronchial tissue.

The alpha1 subunit also showed evidence of high expression in lung tumors.

Inhibition was observed at 100 nM alpha-bungarotoxin (alpha-BTX) or 10 microM hexamethonium (HEX); maximal inhibition was achieved using a combination of alpha-BTX and HEX.

Akt was also phosphorylated in NSCLC cells after exposure to nicotine; this effect was inhibited by the PI3K inhibitor LY294002 and antagonists to the neuronal-type nAChR, but not to the muscle-type receptor.

Nicotine triggered influx of calcium in the 273T NSCLC cell line, suggesting that L-type calcium channels were activated.

273T cells also showed greater activation of p44/42 MAPK than of Akt in response to nicotine.

Cultures treated with nicotine and the EGFR tyrosine kinase inhibitor gefitinib showed a significant increase in the number of surviving cells compared to gefitinib alone.

These data indicate that the muscle-type nAChR, rather than the alpha7 type, is highly expressed in NSCLC and leads to downstream activation of the p44/42 MAPK pathway.

Neuronal-type receptors are also present and functional, as evidenced by antagonist studies, although, the expression levels are lower than muscle-type nAChR.

Nicotine may play a role in regulating survival of NSCLC cells and endogenous acetylcholine released locally in the lung and/or chronic nicotine exposure might play a role in NSCLC development.

[MeSH-major] Ganglionic Stimulants / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Nicotine / pharmacology. Nicotinic Agonists / pharmacology. Protein Subunits / genetics. Receptors, Nicotinic / genetics

[MeSH-minor] Acetylcholine / metabolism. Calcium Channels, L-Type / drug effects. Calcium Channels, L-Type / metabolism. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. alpha7 Nicotinic Acetylcholine Receptor

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(PMID = 17015027.001).

[ISSN] 1094-5539

[Journal-full-title] Pulmonary pharmacology & therapeutics

[ISO-abbreviation] Pulm Pharmacol Ther

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P50 CA090440

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CHRNA1 protein, human; 0 / CHRNB1 protein, human; 0 / Calcium Channels, L-Type; 0 / Chrna7 protein, human; 0 / Ganglionic Stimulants; 0 / Nicotinic Agonists; 0 / Protein Subunits; 0 / RNA, Messenger; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 6M3C89ZY6R / Nicotine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; N9YNS0M02X / Acetylcholine

   

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[Title] Tumor necrosis factor alpha represses bone morphogenetic protein (BMP) signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.

Bone morphogenetic proteins (BMPs) induce not only bone formation in vivo but also osteoblast differentiation of mesenchymal cells in vitro.

Tumor necrosis factor alpha (TNFalpha) inhibits both osteoblast differentiation and bone formation induced by BMPs.

In this study, we found that TNFalpha inhibited the alkaline phosphatase activity and markedly reduced BMP2- and Smad-induced reporter activity in MC3T3-E1 cells.

These results suggest that TNFalpha inhibits BMP signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.

[MeSH-major] Bone Morphogenetic Protein 2 / metabolism. Cell Nucleus / metabolism. Signal Transduction / physiology. Smad Proteins / metabolism. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Active Transport, Cell Nucleus / drug effects. Animals. Cell Line. Mice. Mice, Knockout. Nitriles / pharmacology. Sulfones / pharmacology

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(PMID = 19854828.001).

[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 / 3-(4-methylphenylsulfonyl)-2-propenenitrile; 0 / Bmp2 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Nitriles; 0 / Rela protein, mouse; 0 / Smad Proteins; 0 / Sulfones; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha

[Other-IDs] NLM/ PMC2791026

   

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[Title] Activated G(alpha)13 impairs cell invasiveness through p190RhoGAP-mediated inhibition of RhoA activity.

The GTPase RhoA is a downstream target of heterotrimeric G(13) proteins and plays key roles in cell migration and invasion.

Here, we show that expression in human melanoma cells of a constitutively active, GTPase-deficient Galpha(13) form (G(alpha)(13)QL) or lysophosphatidylcholine (LPC)-promoted signaling through G(alpha)(13)-coupled receptors led to a blockade of chemokine-stimulated RhoA activation and cell invasion that was rescued by active RhoA.

Melanoma cells expressing G(alpha)(13)QL or cells stimulated with LPC displayed an increase in p190RhoGAP activation, and defects in RhoA activation and invasion were recovered by knocking down p190RhoGAP expression, thus identifying this GTPase-activating protein (GAP) protein as a downstream G(alpha)(13) target that is responsible for these inhibitory responses.

In addition, defective stress fiber assembly and reduced migration speed underlay inefficient invasion of G(alpha)(13)QL melanoma cells.

Importantly, G(alpha)(13)QL expression in melanoma cells led to impairment in lung metastasis associated with prolonged survival in SCID mice.

The data indicate that G(alpha)(13)-dependent downstream effects on RhoA activation and invasion tightly depend on cell type-specific GAP activities and that G(alpha)(13)-p190RhoGAP signaling might represent a potential target for intervention in melanoma metastasis.

[MeSH-major] GTP-Binding Protein alpha Subunits, G12-G13 / physiology. Guanine Nucleotide Exchange Factors / physiology. Melanoma / pathology. Repressor Proteins / physiology. rhoA GTP-Binding Protein / antagonists & inhibitors

[MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL12 / pharmacology. GTP-Binding Protein alpha Subunits, Gi-Go / physiology. Humans. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Lysophosphatidylcholines / pharmacology. Mice. Mice, SCID. Neoplasm Invasiveness. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction. Swiss 3T3 Cells. Thromboxane A2 / physiology

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(PMID = 18922893.001).

[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 / ARHGAP35 protein, human; 0 / Chemokine CXCL12; 0 / Guanine Nucleotide Exchange Factors; 0 / Lysophosphatidylcholines; 0 / Proto-Oncogene Proteins c-vav; 0 / Repressor Proteins; 0 / VAV2 protein, human; 57576-52-0 / Thromboxane A2; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, G12-G13; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.2 / rhoA GTP-Binding Protein

   

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[Title] Differential effects of lipoprotein lipase on tumor necrosis factor-alpha and interferon-gamma-mediated gene expression in human endothelial cells.

In vascular diseases, such as atherosclerosis, inflammation plays an important role in the pathogenesis of the disease.

We examined the role of LPL in modulating tumor necrosis factor-alpha (TNF-alpha)- and interferon-gamma (IFN-gamma)-mediated inflammatory cytokine signal transduction pathways in human aortic endothelial cells (HAECs).

LPL significantly suppressed TNF-alpha-induced gene expression, and this suppression was reversed by tetrahydrolipstatin and heparinase.

The anti-inflammatory response of LPL in suppressing TNF-alpha-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-alpha degradation and phosphorylation of the p65 subunit.

[MeSH-major] Endothelial Cells / physiology. Gene Expression Regulation. Interferon-gamma / metabolism. Lipoprotein Lipase / metabolism. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Aorta / cytology. Cholesterol, VLDL / metabolism. Culture Media, Serum-Free. Cytokines / metabolism. DNA-Binding Proteins / metabolism. E-Selectin / metabolism. Enzyme Inhibitors / metabolism. Heparin Lyase / metabolism. Humans. Intercellular Adhesion Molecule-1 / genetics. Intercellular Adhesion Molecule-1 / metabolism. Lactones / metabolism. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism. STAT1 Transcription Factor. Signal Transduction / physiology. Trans-Activators / metabolism. Vascular Cell Adhesion Molecule-1 / metabolism

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(PMID = 15994321.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Grant] United States / NHLBI NIH HHS / HL / HL55667; United States / NHLBI NIH HHS / HL / HL58660; United States / NHLBI NIH HHS / HL / HL70816; United States / NHLBI NIH HHS / HL / HL78615

[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 / Cholesterol, VLDL; 0 / Culture Media, Serum-Free; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Lactones; 0 / NF-kappa B; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / Trans-Activators; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma; 95M8R751W8 / orlistat; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.1.34 / Lipoprotein Lipase; EC 4.2.2.7 / Heparin Lyase

   

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[Title] Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy.

The prehepatic insulin secretion rate was estimated by deconvolution of C-peptide concentrations, and insulin sensitivity (SIRd) was estimated by the glucose clamp technique.

The disposition index (Di=ISREG0-10 min x SIRd) was calculated to estimate the beta-cell response relative to insulin sensitivity.

RESULTS: FISR was increased by 69% (P<0.001), whereas median Di was decreased by 75% (P<0.01), primarily as a result of a reduction of SI(Rd) by 60% (P<0.001) in LIPO patients compared with controls.

Four LIPO patients displayed high FISR [+3 standard deviations (SD), P<0.001], high ISREG0-10 min (+3 SD, P<0.001) and low SIRd (P<0.01), suggesting an intact B-cell capacity to compensate insulin resistance; six LIPO patients exhibited high FISR (+3SD, P<0.001), low ISREG0-10min (-1 SD, P=0.01), and low SIRd (P<0.01), suggesting depletion of readily releasable insulin stores; the remaining eight LIPO patients and controls displayed identical FISR and ISREG0-10 min.

Increased concentrations of the nonglucose insulin secretagogues triglyceride (+124%), alanine (+35%) and glucagon (+88%), and also lactate (+96%) and tumour necrosis factor (TNF)-alpha (+62%) were observed in the 10 LIPO patients with aberrations in FISR and ISREG0-10 min compared with the remaining HIV-infected patients (all P<0.05).

CONCLUSION: Plasma triglyceride, alanine, glucagon, lactate and TNF-alpha may be associated with alterations in the first-phase prehepatic insulin secretion response to intravenous glucose in normoglycaemic lipodystrophic HIV-infected patients.

[MeSH-major] Glucose. HIV-1. HIV-Associated Lipodystrophy Syndrome / metabolism. Insulin / secretion. Insulin Resistance

[MeSH-minor] Adult. Alanine / blood. C-Peptide / analysis. Case-Control Studies. Glucagon / blood. Glucose Clamp Technique. Humans. Infusions, Intravenous. Insulin-Secreting Cells / secretion. Lactates / blood. Male. Middle Aged. Stimulation, Chemical. Triglycerides / blood. Tumor Necrosis Factor-alpha / analysis

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(PMID = 16494630.001).

[ISSN] 1464-2662

[Journal-full-title] HIV medicine

[ISO-abbreviation] HIV Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / C-Peptide; 0 / Insulin; 0 / Lactates; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose; OF5P57N2ZX / Alanine

   

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[Title] Epidermal growth factor ligand/receptor loop and downstream signaling activation pattern in completely resected nonsmall cell lung cancer.

BACKGROUND: In recent years, molecular insights shed light on the role of the epidermal growth factor receptor (EGFR) in nonsmall cell lung cancer (NSCLC), and new therapeutic agents, such as the EGFR tyrosine kinase inhibitors, were tested successfully, with responsiveness to those agents more likely in those patients with specific EGFR gene alterations.

The objective of the current study was to investigate the protein profiles of EGFR, c-erb-B2, transforming growth factor alpha (TGF-alpha) (one of the EGFR ligands commonly expressed in NSCLC), and some downstream molecules, potentially to detect a subset of tumors with an activated autocrine loop that is responsible for higher intracellular signaling.

METHODS: One hundred twelve consecutive patients with resected NSCLC were analyzed by immunohistochemistry for EGFR, the c-erb-B2 receptor, TGF-alpha, and pivotal molecules downstream from EGFR activation.

RESULTS: EGFR, c-erb-B2, TGF-alpha and downstream molecule expression, per se, was not correlated significantly with any clinicopathologic variables, with the exception of a significant correlation between squamous histology and EGFR and between adenocarcinoma and TGF-alpha.

However, nearly 30% of NSCLCs demonstrated coexpression of both TGF-alpha and EGFR, and this molecular status was associated positively with a statistically significant expression of phosphatidylinositol 3 kinase and an inversely with mitogen-activated protein kinase expression.

CONCLUSIONS: The presence of a subgroup of NSCLCs with an activated autocrine loop may help to explain the mechanisms that lead to the relative ineffectiveness of the EGFR tyrosine kinase inhibitor and may support new clinical trials to define whether the subgroup of patients with these tumors reasonably may benefit from higher doses of such inhibitors or from the simultaneous inhibition of EGFR downstream signaling targets.

[MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / surgery. Lung Neoplasms / metabolism. Lung Neoplasms / surgery. Receptor, Epidermal Growth Factor / metabolism

[MeSH-minor] Aged. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Italy. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Receptor, ErbB-2 / metabolism. Retrospective Studies. Signal Transduction. Transforming Growth Factor alpha / metabolism

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[Copyright] (c) 2007 American Cancer Society.

(PMID = 17647268.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.24 / Mitogen-Activated Protein Kinases

   

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[Title] Alpha fetoprotein is a novel protein-binding partner for caspase-3 and blocks the apoptotic signaling pathway in human hepatoma cells.

Although there is increasing evidence that alpha fetoprotein (AFP) may function as regulatory factor in the growth of tumor cells, the precise mechanism is still unclear.

Our results showed that low doses of TNF-related apoptosis-inducing ligand (TRAIL) elevated the activity of caspase-8, but not caspase-3.

Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL.

Knockdown of AFP increased the sensitivity of Bel 7402 cells to TRAIL, and thereby, triggered caspase-3 signaling.

The effect of AFP on caspase-3 was further confirmed by transfection of the AFP gene into HLE cells (AFP negative).

Therefore, it is possible that the combination of AFP gene silencing together with ATRA/TRAIL cotreatment will benefit the enhancement of the chemotherapeutic efficiency of these agents on tumors.

[MeSH-major] Apoptosis / physiology. Carcinoma, Hepatocellular / metabolism. Caspase 3 / metabolism. Liver Neoplasms / metabolism. Signal Transduction. alpha-Fetoproteins / metabolism

[MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Caspase 8 / metabolism. Cell Proliferation / drug effects. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. Fluorescence Resonance Energy Transfer. Humans. Immunoprecipitation. Protein Transport. RNA, Small Interfering / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tretinoin / pharmacology. Tumor Cells, Cultured

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[Copyright] Copyright 2008 UICC.

(PMID = 19267404.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / alpha-Fetoproteins; 5688UTC01R / Tretinoin; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8

   

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[Title] Protein kinase C alpha location and the expression of phospho-MEK and MDR1 in hepatitis virus-related hepatocellular carcinoma biopsies.

The purpose of this study was to elucidate the function of protein kinase C (PKC) alpha in human hepatocellular carcinoma (HCC).

Expression of PKCalpha, phospho-MEK and MDR1 was significantly increased in the region of HCC location compared with the non-tumor location.

The HCC tissues were classified as cytosolic type, where PKCalpha was deposited in the cytoplasm in > 50% of cells, or membranous type for others.

The results showed that the higher expression levels of phospho-MEK and MDR1 in HCC location were significantly associated with those patients whose cells were of the membranous type.

The results indicate that elevated expression of MDR1 in HCC patients with non-HCV infection may be mediated through PKC signaling pathway.

[MeSH-major] Carcinoma, Hepatocellular / metabolism. Hepatitis B / complications. Hepatitis C / complications. Liver Neoplasms / metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. P-Glycoprotein / metabolism. Protein Kinase C-alpha / metabolism

[MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cell Membrane / metabolism. Cytoplasm / metabolism. Female. Humans. Male. Middle Aged. Retrospective Studies. Signal Transduction / physiology

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(PMID = 21793318.001).

[ISSN] 0304-4920

[Journal-full-title] The Chinese journal of physiology

[ISO-abbreviation] Chin J Physiol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China (Republic : 1949- )

[Chemical-registry-number] 0 / P-Glycoprotein; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases

   

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[Title] [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation].

Gene P504S is considered as the most specific for prostatic carcinoma and its protein (alpha-methylacyl coenzyme A racemaze (AMACR/P504S) is higly sensitive and specific marker not only for adenocarcinoma cells but also for preceding changes - prostatic intraepithelial neoplasm (PIN).

AMACR/P504S seems to be the first marker of malignant transformation and tumor progression.

Use of immunohistochemical method for revealing this marker together with methods of basal prostatic cells observation (cytokeratin of a high molecular weight, cytokeratin 5/6, p63) improves morphological diagnosis of prostatic carcinoma, particularly on the material of needle biopsies.

This combination allows one to identify neoplastic nature of some difficult lesions.

[MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / analysis

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(PMID = 16323473.001).

[ISSN] 0004-1955

[Journal-full-title] Arkhiv patologii

[ISO-abbreviation] Arkh. Patol.

[Language] rus

[Publication-type] Editorial; English Abstract

[Publication-country] Russia (Federation)

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

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[Title] Effects of estradiol on lipopolysaccharide and Pam3Cys stimulation of CCL20/macrophage inflammatory protein 3 alpha and tumor necrosis factor alpha production by uterine epithelial cells in culture.

We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3alpha) and tumor necrosis factor alpha (TNF-alpha) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys.

To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3alpha and TNF-alpha secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h.

E2 inhibited the constitutive secretion of TNF-alpha and CCL20/MIP3alpha into culture media.

In contrast, and at the same time, E2 lowered the TNF-alpha response to both PAMP.

To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist.

ICI 182,780 had no effect on E2 inhibition of constitutive TNF-alpha and CCL20/MIP3alpha secretion.

In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3alpha secretion as well as partially reversed the inhibitory effect of E2 on TNF-alpha production by epithelial cells.

Overall, these results indicate that E2 regulates the production of TNF-alpha and CCL20/MIP3alpha by UEC in the absence as well as presence of PAMP.

Since CCL20/MIP3alpha has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3alpha and TNF-alpha by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.

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(PMID = 15972514.001).

[ISSN] 0019-9567

[Journal-full-title] Infection and immunity

[ISO-abbreviation] Infect. Immun.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / AI-13541; United States / NIAID NIH HHS / AI / R01 AI013541; United States / NIAID NIH HHS / AI / R37 AI013541; United States / NIAID NIH HHS / AI / P01 AI051877; United States / NIAID NIH HHS / AI / AI-51877

[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 / Ccl20 protein, rat; 0 / Chemokine CCL20; 0 / Chemokines, CC; 0 / Lipopolysaccharides; 0 / Lipoproteins; 0 / Macrophage Inflammatory Proteins; 0 / Tumor Necrosis Factor-alpha; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 87420-41-5 / 2,3-bis(palmitoyloxy)-2-propyl-1-palmitoylcysteine; K848JZ4886 / Cysteine

[Other-IDs] NLM/ PMC1168574

   

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[Title] Naftopidil, a selective alpha-1 adrenoceptor antagonist, inhibits growth of human prostate cancer cells by G1 cell cycle arrest.

Alpha-1 adrenoceptor antagonists are generally prescribed for benign prostate hyperplasia with lower urinary tract symptoms.

Naftopidil, a selective alpha-1 adrenoceptor antagonist, is frequently used in Japan because it has fewer side effects.

Here we demonstrate for the first time that naftopidil has growth inhibitory effect in androgen-sensitive and -insensitive human prostate cancer cell lines.

The concentrations causing 50% inhibition (IC50) of cancer cell growth were 22.2 +/- 4.0 microM in androgen-sensitive LNCaP cells and 33.2 +/- 1.1 microM in androgen-insensitive PC-3 cells.

FACS analysis revealed that cell growth inhibition by naftopidil was due to the arrest of the G1 cell cycle.

Expressions of p27(kip1) and p21(cip1) were significantly increased in LNCaP cells treated with naftopidil.

In PC-3 cells, naftopidil induced p21(cip1) but not p27(kip1).

In vivo, oral administration of naftopidil to nude mice inhibited the growth of PC-3 tumors as compared to vehicle-treated controls.

These results suggest that naftopidil may be useful in the chemoprevention of prostate cancer and the intervention of hormone refractory prostate cancer.

[MeSH-major] Adrenergic alpha-1 Receptor Antagonists. G1 Phase / drug effects. Naphthalenes / pharmacology. Piperazines / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism

[MeSH-minor] Adrenergic alpha-Antagonists / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation. Cell Separation. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Flow Cytometry. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Male. Mice. Mice, Nude. Neoplasm Transplantation. Receptors, Adrenergic, alpha-1 / metabolism

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[Copyright] Copyright 2007 Wiley-Liss, Inc.

(PMID = 17918159.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Intracellular Signaling Peptides and Proteins; 0 / Naphthalenes; 0 / Piperazines; 0 / Receptors, Adrenergic, alpha-1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; R9PHW59SFN / naftopidil

   

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[Title] Tumor necrosis factor-alpha-induced anterior pituitary folliculostellate TtT/GF cell uncoupling is mediated by connexin 43 dephosphorylation.

The anterior pituitary folliculostellate (FS) cells are key elements of the paracrine control of the pituitary function.

These cells are the source and the target of growth factors and cytokines, and are connected to other pituitary cells via Cx43-mediated gap junctions.

Here, we show that acute treatment of the FS TtT/GF cell line with TNF-alpha caused a transient cell uncoupling that was accompanied by the dephosphorylation of Cx43 in Ser368.

These TNF-alpha-evoked effects were dependent on protein phosphatase 2A (PP2A) and protein kinase C (PKC) activities.

TNF-alpha did not affect total cell Cx43-PP2A catalytic subunit interaction, but it did induce PP2A catalytic subunit recruitment to the Triton X-100 insoluble subcellular fraction, in which Cx43-gap junction plaques are recovered.

Cx43 did not interact with the conventional PKC-alpha, but it did interact with the atypical PKC-zeta.

Moreover, this interaction was weakened by TNF-alpha.

The temporary closure of gap junctions during acute TNF-alpha challenge may constitute a protective mechanism to limit or confine the spread of inflammatory signals among the FS cells.

[MeSH-major] Connexin 43 / metabolism. Pituitary Gland, Anterior / drug effects. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology

[MeSH-minor] Animals. Blotting, Western. Cell Communication / drug effects. Cell Line. Gap Junctions / drug effects. Gap Junctions / metabolism. Isoenzymes / metabolism. Mice. Microscopy, Fluorescence. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Protein Binding. Protein Kinase C / metabolism. Protein-Serine-Threonine Kinases / metabolism. Time Factors. Tyrosine / metabolism

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(PMID = 17872368.001).

[ISSN] 0013-7227

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Connexin 43; 0 / Isoenzymes; 0 / Tumor Necrosis Factor-alpha; 42HK56048U / Tyrosine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.13 / Protein Kinase C; EC 3.1.3.16 / Phosphoprotein Phosphatases

   

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[Title] Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice.

In recent years, the outcome has been globally improved by current therapies, but it remains poor in patients with high, persistent residual disease following the first course of chemotherapy, prompting evaluation of the possible beneficial effects of immunotherapy protocols.

In this study, we hypothesized that the disruption of two immunoregulatory pathways controlling the auto-reactive T cell response might synergize with dendritic cell-based immunotherapy of the disease, which is considered to be poorly immunogenic.

In this study, we used TAL1xLMO1 leukemia cells adoptively transferred in mice, to generate murine leukemia with poorly immunogenic cells as a model for human T-ALL.

We compared the efficiency of a classical, dendritic cell-based immunotherapy (injection of dendritic cells loaded with tumor-derived antigenic products), to a combined treatment associating injection of antigen-loaded dendritic cells and disruption of the two immunoregulatory pathways: CD25+ suppressive T cells and cytotoxic T lymphocyte-associated antigens (CTLA-4).

We show that this combined treatment resulted in cure, concomitantly with in vivo generation of immune memory, and TNF-alpha secretion.

This study demonstrates that the disruption of these two immunoregulatory pathways synergized with immunostimulation by dendritic cells loaded with tumor-derived antigens, and paves the way for the testing of this combination in clinical trials.

[MeSH-major] Immunotherapy, Adoptive. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes / immunology

[MeSH-minor] Animals. Antigens, CD / metabolism. Antigens, Neoplasm / administration & dosage. CTLA-4 Antigen. Cell Line, Tumor. Dendritic Cells / immunology. Dendritic Cells / metabolism. Dendritic Cells / transplantation. Disease Models, Animal. Immunologic Memory. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphocyte Depletion. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism. Tumor Necrosis Factor-alpha / secretion

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(PMID = 16464745.001).

[ISSN] 1148-5493

[Journal-full-title] European cytokine network

[ISO-abbreviation] Eur. Cytokine Netw.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Ctla4 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein.

LIM domain only 4 (LMO4), a member of the LIM-only family of transcriptional coregulatory proteins, consists of two LIM protein-protein interaction domains that enable it to function as a linker protein in multiprotein complexes.

Here, we have identified estrogen receptor alpha (ERalpha) and its corepressor, metastasis tumor antigen 1 (MTA1), as two novel binding partners of LMO4.

Interestingly, LMO4 exhibited binding with both ERalpha and MTA1 and existed as a complex with ERalpha, MTA1, and histone deacetylases (HDAC), implying that LMO4 was a component of the MTA1 corepressor complex.

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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[Title] Notch-1 regulates pulmonary neuroendocrine cell differentiation in cell lines and in transgenic mice.

The notch gene family encodes transmembrane receptors that regulate cell differentiation by interacting with surface ligands on adjacent cells.

Previously, we demonstrated that tumor necrosis factor-alpha (TNF) induces neuroendocrine (NE) cell differentiation in H82, but not H526, undifferentiated small cell lung carcinoma lines.

We now test the hypothesis that TNF mediates NE cell differentiation in part by altering Notch gene expression.

First, using RT-PCR, we determined that TNF treatment of H82, but not H526, transiently decreases notch-1 mRNA in parallel with induction of gene expression for the NE-specific marker DOPA decarboxylase (DDC).

After 7 days of Notch-1 antisense treatment, neural cell adhesion molecule (NCAM) immunoreactivity is induced in H82 but not H526.

Third, we generated transgenic mice bearing notch-1 driven by the neural/NE-specific calcitonin promoter, which express activated Notch-1 in developing lung epithelium.

Newborn NotchCal mouse lungs have high levels of hes1 mRNA, reflecting increased activated Notch, compared with wild-type.

NotchCal lungs have decreased CGRP-positive NE cells, decreased protein gene product 9.5 (PGP9.5)-positive NE cells, and decreased gastrin-releasing peptide (GRP), CGRP, and DDC mRNA levels compared with normal littermates.

Cumulatively, these observations provide further support for a role for Notch-1 signaling in regulating pulmonary NE cell differentiation.

[MeSH-major] Cell Differentiation. Lung / cytology. Neurosecretory Systems / cytology. Receptor, Notch1 / metabolism

[MeSH-minor] Animals. Animals, Newborn. Calcitonin / genetics. Carcinoma, Small Cell / genetics. Carcinoma, Small Cell / pathology. Cell Line, Tumor. Dopa Decarboxylase / genetics. Gastrin-Releasing Peptide / genetics. Gastrin-Releasing Peptide / metabolism. Gene Expression / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mice. Mice, Transgenic. Neural Cell Adhesion Molecules / metabolism. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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(PMID = 17028268.001).

[ISSN] 1040-0605

[Journal-full-title] American journal of physiology. Lung cellular and molecular physiology

[ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.

[Language] eng

[Grant] United States / NHLBI NIH HHS / HL / R01-HL-44984

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Tumor Necrosis Factor-alpha; 80043-53-4 / Gastrin-Releasing Peptide; 9007-12-9 / Calcitonin; EC 4.1.1.- / Dopa Decarboxylase

   

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[Title] Vascular smooth muscle cell calcification and SLC20 inorganic phosphate transporters: effects of PDGF, TNF-alpha, and Pi.

Pi transport by vascular smooth muscle cells (VSMC) has been proposed to play an important role in the pathogenesis of vascular calcification.

In this study, we have determined the correlation between calcification induced by Pi, platelet-derived growth factor (PDGF)-BB, and tumor necrosis factor-alpha and Pi transport activity in primary cultures of rat aortic VSMC.

Only PDGF increased Pi transport when it was expressed per unit of DNA, as PDGF also increased total cell protein by 100%, while DNA content and number of cells were not modified.

PDGF increased the expression of the Pi transporter, Pit-1, but membrane protein biotinylation showed that Pit-1 abundance was not modified in the cell surface.

Immunofluorescence revealed that, under basal conditions, Pit-1 is only slightly expressed at the cell membrane, but strongly expressed inside the cell.

The intracellular signal colocalizes with endoplasmic reticulum (ER) markers, and PDGF increases Pit-1 expression in the ER but not the cell membrane.

In conclusion, Pi transport across the plasma membrane does not correlate directly with calcification, but the expression of Pit-1 in the ER opens new possibilities for the study of the pathogenesis of vascular calcification.

[MeSH-major] Muscle, Smooth, Vascular / metabolism. Phosphates / pharmacology. Platelet-Derived Growth Factor / pharmacology. Sodium-Phosphate Cotransporter Proteins, Type III / physiology. Tumor Necrosis Factor-alpha / pharmacology

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(PMID = 19506901.001).

[ISSN] 1432-2013

[Journal-full-title] Pflugers Archiv : European journal of physiology

[ISO-abbreviation] Pflugers Arch.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / 1 R01 DK066029

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Phosphates; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Slc20a1 protein, rat; 0 / Sodium-Phosphate Cotransporter Proteins, Type III; 0 / Tumor Necrosis Factor-alpha; 1B56C968OA / becaplermin

   

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[Title] Fibroblasts isolated from common sites of breast cancer metastasis enhance cancer cell growth rates and invasiveness in an interleukin-6-dependent manner.

Common sites of breast cancer metastasis include the lung, liver, and bone, and of these secondary metastatic sites, estrogen receptor alpha (ERalpha)-positive breast cancer often favors bone.

Within secondary organs, cancer cells would predictably encounter tissue-specific fibroblasts or their soluble factors, yet our understanding of how tissue-specific fibroblasts directly affect cancer cell growth rates and survival remains largely unknown.

Therefore, we tested the hypothesis that mesenchymal fibroblasts isolated from common sites of breast cancer metastasis provide a more favorable microenvironment with respect to tumor growth rates.

We found a direct correlation between the ability of breast, lung, and bone fibroblasts to enhance ERalpha-positive breast cancer cell growth and the level of soluble interleukin-6 (IL-6) produced by each organ-specific fibroblast, and fibroblast-mediated growth enhancement was inhibited by the removal or inhibition of IL-6.

Interestingly, mice coinjected with MCF-7 breast tumor cells and senescent skin fibroblasts, which secrete IL-6, developed tumors, whereas mice coinjected with presenescent skin fibroblasts that produce little to no IL-6 failed to form xenograft tumors.

We subsequently determined that IL-6 promoted growth and invasion of breast cancer cells through signal transducer and activator of transcription 3-dependent up-regulation of Notch-3, Jagged-1, and carbonic anhydrase IX.

These data suggest that tissue-specific fibroblasts and the factors they produce can promote breast cancer disease progression and may represent attractive targets for development of new therapeutics.

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(PMID = 18974155.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA109451; 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-116199

[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 / Culture Media, Conditioned; 0 / Interleukin-6; 0 / STAT3 Transcription Factor

   

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[Title] Exposure to cigarette smoke upregulates AP-1 activity and induces TNF-alpha overexpression in mouse lungs.

Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease, and involves overexpression of many proinflammatory genes.

Transcription factors regulating expression of inflammatory mediators may play a key role in characterizing the disease.

The levels of inflammatory mediators tumor necrosis factor (TNF)-alpha, interleukin(IL)-6, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured using enzyme-linked immunosorbent assay (ELISA).

Compared to the control group, smoke exposure induced a notable increase in TNF-alpha in BALF.

These data demonstrated that subacute smoke-triggered lung inflammation was accompanied by inflammatory cell influx, AP-1 activation, and proinflammatory gene overexpression in mouse lungs.

[MeSH-major] Gene Expression Regulation / physiology. Lung / metabolism. Smoking / metabolism. Transcription Factor AP-1 / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis. Up-Regulation / physiology

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(PMID = 19235541.001).

[ISSN] 1091-7691

[Journal-full-title] Inhalation toxicology

[ISO-abbreviation] Inhal Toxicol

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Inflammation Mediators; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Antisense RNA to inducible nitric oxide synthase reduces cytokine-mediated brain endothelial cell death.

We test whether inhibition of inducible nitric oxide synthase (iNOS) can exert a cytoprotective effect on cerebral endothelial cells upon stimulation by pro-inflammatory cytokines.

Mouse brain endothelial cells were stably transfected to express an antisense RNA against iNOS driven by an endothelium-specific von Willebrand factor (vWF) promoter.

Upon stimulation with tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma), antisense transfectants showed less iNOS enzymatic activity with less nitric oxide (NO) when compared to the sense control cells.

Correspondingly, the antisense cells showed a reduced LDH release and less cytosolic content of oligonucleosomes.

These findings establish a cell-specific antisense strategy and confirm the cytotoxic role of iNOS expression in cultured cerebral endothelial cells.

[MeSH-major] Brain / cytology. Brain / metabolism. Cytokines / pharmacology. Endothelial Cells / cytology. Endothelial Cells / metabolism. Nitric Oxide Synthase Type II / metabolism. RNA, Antisense / genetics

[MeSH-minor] Animals. Cell Death / drug effects. Cell Line. Mice

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(PMID = 15965090.001).

[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 / Cytokines; 0 / RNA, Antisense; EC 1.14.13.39 / Nitric Oxide Synthase Type II

   

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[Title] The effect of cyclosporin on cell division and apoptosis in human oral keratinocytes.

The objective of the present study was to investigate the effects of CsA on the growth of oral epithelial cells in vitro and to test the hypothesis that CsA influences apoptosis in these cells.

MATERIAL AND METHODS: Cyclosporin was cocultured with an immortalized normal human oral keratinocyte cell line (HOK-16B), an epitheloid cervical carcinoma cell line (HeLa) and primary oral keratinocytes.

Cell division was quantified using a CyQUANT kit.

Apoptosis was induced using tumour necrosis factor-alpha (TNF-alpha) and assayed by analysis of caspase-3 activity.

RESULTS: CsA exhibited a dose- and time-dependent inhibition of cell division in all three keratinocyte cell cultures.

Significantly, HOK-16B cells treated with high doses of CsA (10 alphag/ml) did not recover their proliferative capacity 3 d after withdrawal of CsA, indicating that CsA-induced inhibition of growth is not temporary.

Concentrations of CsA that inhibited cell division (1 microg/ml) did not have any effect on constitutive or TNF-alpha -induced apoptosis or Bcl-2 expression in HOK-16B cells.

CONCLUSION: CsA inhibits oral epithelial cell division and this effect is not associated with changes in apoptosis in these cells.

The action of CsA on oral epithelial cells may be associated with a long-lasting stress signal, which might account for some of the pathological effects of this drug.

[MeSH-minor] Caspase 3. Caspases / metabolism. Cell Line, Transformed. Cell Proliferation / drug effects. HeLa Cells. Humans. Proto-Oncogene Proteins c-bcl-2 / biosynthesis

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(PMID = 16827723.001).

[ISSN] 0022-3484

[Journal-full-title] Journal of periodontal research

[ISO-abbreviation] J. Periodont. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Denmark

[Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases

   

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[Title] Contribution of adipocyte-derived factors to beta-cell dysfunction in diabetes.

In addition to serving as an energy reservoir, the adipocyte has been characterized as an endocrine cell, secreting many bioactive factors which influence energy homeostasis.

Being overweight, with excessive adipose tissue, is considered to be part of the pathogenesis of type 2 diabetes.

Insulin resistance and beta-cell dysfunction are two major pathophysiological changes seen in type 2 diabetes.

In addition to inducing insulin resistance in insulin-responsive tissues, adipocyte-derived factors play an important role in the pathogenesis of beta-cell dysfunction.

Leptin, free fatty acids, adiponectin, tumor necrosis factor-alpha and interleukin-6 are all produced and secreted by adipocytes, and may directly influence aspects of beta-cell function, including insulin synthesis and secretion, insulin cell survival and apoptosis.

During the progression from normal weight to obesity and on to overt diabetes, the adipocyte-derived factors contribute to the occurrence and development of beta-cell dysfunction and type 2 diabetes.

[MeSH-major] Adipocytes / physiology. Diabetes Mellitus / physiopathology. Insulin-Secreting Cells / drug effects

[MeSH-minor] Adiponectin / physiology. Animals. Fatty Acids, Nonesterified / physiology. Humans. Interleukin-6 / physiology. Leptin / physiology. Tumor Necrosis Factor-alpha / physiology

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(PMID = 16378747.001).

[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; Review

[Publication-country] England

[Chemical-registry-number] 0 / Adiponectin; 0 / Fatty Acids, Nonesterified; 0 / Interleukin-6; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha

[Number-of-references] 155

   

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[Title] Endothelial and virgultar cell formations in the mammalian lymph node sinus: endothelial differentiation morphotypes characterized by a special kind of junction (complexus adhaerens).

The lymph node sinus are channel structures of unquestionable importance in immunology and pathology, specifically in the filtering of the lymph, the transport and processing of antigens, the adhesion and migration of immune cells, and the spread of metastatic cancer cells.

Our knowledge of the cell and molecular biology of the sinus-forming cells is still limited, and the origin and biological nature of these cells have long been a matter of debate.

Here, we review the relevant literature and present our own experimental results, in particular concerning molecular markers of intercellular junctions and cell differentiation.

We show that both the monolayer cells lining the sinus walls and the intraluminal virgultar cell meshwork are indeed different morphotypes of the same basic endothelial cell character, as demonstrated by the presence of a distinct spectrum of general and lymphatic endothelial markers, and we therefore refer to these cells as sinus endothelial/virgultar cells (SEVCs).

These cells are connected by unique adhering junctions, termed complexus adhaerentes, characterized by the transmembrane glycoprotein VE-cadherin, combined with the desmosomal plaque protein desmoplakin, several adherens junction plaque proteins including alpha- and beta-catenin and p120 catenin, and components of the tight junction ensemble, specifically claudin-5 and JAM-A, and the plaque protein ZO-1.

Overall, the SEVC system might be considered as a local and specific modification of the general lymphatic vasculature system.

Finally, physiological and pathological alterations of the SEVC system will be presented, and the possible value of the molecular markers described in histological diagnoses of autochthonous lymph node tumors will be discussed.

[MeSH-major] Adherens Junctions / metabolism. Desmosomes / metabolism. Endothelial Cells / metabolism. Lymph Nodes / metabolism. Lymphatic Vessels / metabolism. Tight Junctions / metabolism

[MeSH-minor] Animals. Antigens, Differentiation. Biological Transport. Cell Adhesion. Cell Differentiation. Cell Movement. Cytoskeletal Proteins / metabolism. Humans. Lymph / metabolism. Membrane Glycoproteins / metabolism. Neoplasm Metastasis. Neoplasms / metabolism. Neoplasms / pathology

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(PMID = 19015886.001).

[ISSN] 1432-0878

[Journal-full-title] Cell and tissue research

[ISO-abbreviation] Cell Tissue Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cytoskeletal Proteins; 0 / Membrane Glycoproteins

[Number-of-references] 202

   

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[Title] Mechanism of cancer cell adaptation to metabolic stress: proteomics identification of a novel thyroid hormone-mediated gastric carcinogenic signaling pathway.

To determine the mechanism of adaptation to metabolic stress in cancer cells, we used gastric cancer as a model system to reveal the potential signaling pathways involved.

Two-dimensional polyacrylamide gel electrophoresis coupled with ESI-Q-TOF MS/MS analysis was used to identify differentially expressed proteins between gastric tumor tissues and the corresponding noncancerous tissues.

T(3)-induced expression of HIF1-alpha and vascular endothelial growth factor was further verified using a gastric cancer cell line and in vivo mouse model.

Because the early accumulation of HIF1-alpha was found to be independent of de novo transcription, we also found that the cytosolic cascade phosphatidylinositol 3-kinase/Akt pathway sensitive to T(3) stimulus was involved.

Furthermore we demonstrated that T(3)-induced overexpression of HIF1-alpha was mediated by fumarate accumulation and could be enhanced by fumarate hydratase inactivation but inhibited by 2-oxoglutarate.

These results provide evidence for alteration of metabolic proteins and dysfunction of thyroid hormone regulation in gastric tumors, and a novel thyroid hormone-mediated tumorigenic signaling pathway is proposed.

Our findings are considered a significant step toward a better understanding of adaptations to metabolic stress in gastric carcinogenesis.

[MeSH-major] Adaptation, Physiological. Proteomics. Signal Transduction. Stomach Neoplasms / metabolism. Stress, Physiological. Thyroid Hormones / metabolism

[MeSH-minor] Animals. Cell Line, Tumor. Citrates / metabolism. Electrophoresis, Gel, Two-Dimensional. Fumarate Hydratase / metabolism. Fumarates / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mass Spectrometry. Mice. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Reproducibility of Results. Triiodothyronine / metabolism. Up-Regulation / drug effects. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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(PMID = 18723843.001).

[ISSN] 1535-9484

[Journal-full-title] Molecular & cellular proteomics : MCP

[ISO-abbreviation] Mol. Cell Proteomics

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Citrates; 0 / Fumarates; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Thyroid Hormones; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 06LU7C9H1V / Triiodothyronine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 4.2.1.2 / Fumarate Hydratase

   

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[Title] Hesperidin inhibits expression of hypoxia inducible factor-1 alpha and inflammatory cytokine production from mast cells.

The citrus unshiu peel has been used traditionally as a medicine to improve bronchial and asthmatic conditions or cardiac and blood circulation in Korea, China, and Japan.

Here, we report the effects of citrus unshiu peel water extract (CPWE) on the phorbol myristate acetate (PMA)+calcium ionophore A23187-induced hypoxia-inducible factor-1alpha (HIF-1alpha) activation and inflammatory cytokine production from the human mast cell line, HMC-1 cells.

CPWE and hesperidin inhibited the PMA+A23187-induced HIF-1alpha expression and the subsequent production of vascular endothelial growth factor (VEGF).

We also show that the increased cytokines interleukin (IL)-1beta, IL-8, and tumor necrosis factor (TNF)-alpha level was significantly inhibited by treatment of CPWE or hesperidin.

In the present study, we report that CPWE and hesperidin are inhibitors of HIF-1alpha and cytokines on the mast cell-mediated inflammatory responses.

[MeSH-major] Cytokines / metabolism. Hesperidin / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Inflammation Mediators / metabolism. Mast Cells / drug effects. Mast Cells / metabolism

[MeSH-minor] Calcimycin / pharmacology. Cell Survival / drug effects. Cells, Cultured. Citrus / chemistry. Drugs, Chinese Herbal / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression / drug effects. HL-60 Cells. HeLa Cells. Humans. Ionophores / pharmacology. Tetradecanoylphorbol Acetate / pharmacology. Vascular Endothelial Growth Factor A / metabolism

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(PMID = 17629775.001).

[ISSN] 0300-8177

[Journal-full-title] Molecular and cellular biochemistry

[ISO-abbreviation] Mol. Cell. Biochem.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Cytokines; 0 / Drugs, Chinese Herbal; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inflammation Mediators; 0 / Ionophores; 0 / Vascular Endothelial Growth Factor A; 37H9VM9WZL / Calcimycin; E750O06Y6O / Hesperidin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate

   

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[Title] Inflammatory cytokines and cell adhesion molecules in a rat model of decompression sickness.

Early blood and tissue markers predictive of DCS include inflammatory cytokines and cell adhesion molecules (CAMs).

Increased levels of inflammatory cytokines, especially tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interferon-gamma (IFN-gamma), were detected in the circulation 6 h after decompression.

Compared with control animals maintained at 1 atmospheres absolute pressure ATA (101 kPascal), significant increases in expression of E-selectin, and L-selectin, as well as intercellular adhesion molecule-1 (ICAM-1), were observed immunohistochemically in the lungs and brains of the rats 6 h after exposure to 2 (203 kPascal), 3 (303 kPascal), or 4 (404 kPascal) ATA, followed by rapid decompression.

In contrast to the observations in brain, greater increases in expression of E-selectin and L-selectin around vessels and connective tissue were seen at 24 h after decompression in the quadriceps of rats exposed to either 3 or 4 ATA.

This study demonstrated that rapid decompression induces the release of mediators of inflammation and resulting tissue inflammation cascades, as well as a protective anti-inflammatory response.

[MeSH-major] Cell Adhesion Molecules / metabolism. Cytokines / metabolism. Decompression Sickness / immunology

[MeSH-minor] Animals. Brain / immunology. Disease Models, Animal. E-Selectin / metabolism. Female. Inflammation Mediators / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / blood. Interferon-gamma / metabolism. Interleukin-6 / blood. Interleukin-6 / metabolism. L-Selectin / metabolism. Lung / immunology. Muscle, Skeletal / immunology. Rats. Rats, Sprague-Dawley. Receptor, Adenosine A2A / metabolism. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 18279101.001).

[ISSN] 1079-9907

[Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

[ISO-abbreviation] J. Interferon Cytokine Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / E-Selectin; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma

   

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[Title] Integrated optical biosensor for in-line monitoring of cell cultures.

An analytical detection platform was developed to evaluate the induced toxicity in cell cultures exposed to foreign agents like growth factors or nanoparticles.

Connecting a biosensing detection device to the cell culture flasks allows analyzing the composition of cell medium in real-time.

The analysis relies on the quantification of inflammatory cytokines released by cells into the cell culture medium, by means of solid-phase immunoassays analyzed with the wavelength interrogated optical sensing (WIOS) instrument.

A fluidic system for in situ measurements allows detecting cytokines in real-time, with a sensitivity of 1-100 ng/mL depending on the cytokine.

In addition, integration of an in-line optical absorbance measurement unit, in combination with the standard AB cell proliferation assay, provides information on the cell viability in the culture.

Fluidic connections between the cell culture flasks, the optical biosensor and the absorbance measurement unit simultaneously allow quantifying up to three cytokines (interleukin 8, interleukin 6 and the monocyte chemotactic protein), assessing cellular proliferation, and thus discriminating between naïve cells and cells exposed to foreign agents such as growth factors (tumor necrosis factor alpha) or nanoparticles.

[MeSH-major] Biosensing Techniques / instrumentation. Cell Culture Techniques / instrumentation. Computer Systems

[MeSH-minor] Cell Line. Cell Proliferation / drug effects. Cell Survival. Culture Media / analysis. Cytokines / analysis. Cytokines / biosynthesis. Humans. Immunoassay / methods. Nanoparticles / toxicity. Optical Processes. Spectrophotometry. Tumor Necrosis Factor-alpha / pharmacology

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[Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.

(PMID = 20732803.001).

[ISSN] 1873-4235

[Journal-full-title] Biosensors & bioelectronics

[ISO-abbreviation] Biosens Bioelectron

[Language] eng

[Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Culture Media; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Immunotherapy of hepatocellular carcinoma with a vaccine based on xenogeneic homologous alpha fetoprotein in mice.

alpha-Fetoprotein (AFP) is a diagnostic marker for the presence of hepatocellular carcinoma, and a potential target for immunotherapy.

In the present study, we used AFP as a model antigen to explore the feasibility of the immunotherapy of AFP-positive liver cancer by the breaking of immune tolerance against AFP in a cross-reaction between the xenogeneic homologues and self molecules.

Recombinant rat AFP was prepared as a vaccine, and mouse AFP was prepared as a control.

Both humoral and cellular immune responses may be responsible for the antitumor activity against AFP-positive tumor cells, and no marked side effects were observed in the immunized mice.

[MeSH-major] Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. alpha-Fetoproteins / immunology. alpha-Fetoproteins / therapeutic use

[MeSH-minor] Animals. Antibodies, Neoplasm / blood. Antibodies, Neoplasm / immunology. Cell Line, Tumor. Immune Tolerance. Immunotherapy / methods. Mice. Mice, Inbred C57BL. Rats. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / therapeutic use

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(PMID = 18725206.001).

[ISSN] 1090-2104

[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 / Antibodies, Neoplasm; 0 / Cancer Vaccines; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins

   

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[Title] [Experiment on induction of fibroblasts on 3-D cell-foam structures to express osteoblastic phenotype and its mechanism].

OBJECTIVE: To study the feasibility of osteogenic phenotype expression by human skin fibroblasts induced in polyglycolic acid (PGA) foams and the effect of tumor necrosis factor-alpha (TNF-alpha) on the expression of bone morphogenetic protein (BMP) receptors.

The cell-PGA complexes were cultured in RCCS for 6 weeks, in the media of TNF-alpha (50 U/ml) and BMP-2 (0.1 microg/ml).

1 d, 3 and 6 weeks later, cells and extracellular matrix were investigated by electron microscopic and histochemistry observation respectively.

Secretion of osteogenic markers were analyzed by biochemical methods. (2) Fibroblasts were seeded on the glass fragments or culture flasks and treated with TNF-alpha (50 U/ml) in different usage (one-time, all-time).

The RT-PCR method and the immunohistochemistry fluorescence staining were used to examine the influence of TNF-alpha on the mRNA expression and the protein expression of the type I BMP receptors at 2, 4, 6, 8 d after treatment.

RESULTS: Fibroblasts seeded on the PGA foams formed 3-dimensional matrix 3 weeks after seeding, which was demonstrated as osteo-tissue by tetracycline labeling and ARS staining.

Cells secreted much more bone-specific alkaline phosphatase (B-AKP) and osteocalcin (OCN) into supernatant than the cells that were cultured in the media without TNF-a and BMP2.

Eight days after all-time usage, the TNF-alpha (50 U/ml) increased the expression of the mRNA and protein of the type IB BMP receptor.

CONCLUSIONS: Fibroblasts on 3-D cell-foam structures can express osteoblastic phenotype under certain inducing conditions.

The numerous fibroblasts in body would be a promising resource for cell seeds candidate of tissue- engineered bone.

TNF-alpha provides the essential condition for BMP2's target effect on fibroblasts, and combined use of TNF-alpha and BMP2 is one of the regulating factors.

[MeSH-major] Bone Morphogenetic Protein Receptors, Type I / genetics. Bone Morphogenetic Protein Receptors, Type II / genetics. Bone Morphogenetic Proteins / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Transforming Growth Factor beta / pharmacology. Tumor Necrosis Factor-alpha / pharmacology

[MeSH-minor] Bone Morphogenetic Protein 2. Cell Culture Techniques / methods. Cell Differentiation / drug effects. Cells, Cultured. Drug Synergism. Humans. Phenotype. Polyglycolic Acid

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(PMID = 16635375.001).

[ISSN] 0529-5815

[Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]

[ISO-abbreviation] Zhonghua 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 / BMP2 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / TNF protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 26009-03-0 / Polyglycolic Acid; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II

   

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[Title] The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth.

The influence of alpha-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS) cells of intact Ehrlich carcinoma -bearing CBA mice was studied.

Bone marrow NS cells were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (rho=1.080 g/ml), NS2 (rho=1.090 g/ml) and NS3 (1.100>rho>1.090 g/ml).

These fractions were highly different in their sensitivity to known NS cell inductors (interleukin (IL)-2, IL-3 or histamine).

None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer cell inhibitory) activity under the influence of AFP.

A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer cell activity.

NS activity, especially NS2, was increased in when tumor cells were subcutaneously inoculated three days after AFP injection.

In the AFP-treated mice, the tumor mass at 14 days was 60% larger than that in the untreated mice.

Our data confirmed that AFP is a tumor marker that can inhibit cancer immunity and plays a role in cancer pathogenesis.

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(PMID = 19967055.001).

[ISSN] 2093-3827

[Journal-full-title] The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology

[ISO-abbreviation] Korean J. Physiol. Pharmacol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2788635

[Keywords] NOTNLM ; Alpha-fetoprotein (AFP) / Ehrlich carcinoma (EC) / Natural killer cells / Natural suppressor (NS) cells

   

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[Title] TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis.

Toll-like receptor 3 (TLR3) has gained recognition as a novel molecular target for cancer therapy because TLR3 activation by its synthetic ligand poly I:C directly causes tumor cell death.

Recently, we reported that tumor suppressor p53 increases the expression of TLR3 in several tumor cell lines.

Another study also showed that interferon-alpha (IFN-alpha) up-regulates TLR3 expression.

We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced tumor cell death through the up-regulation of TLR3 expression.

Here, we screened several anticancer drugs that, together with poly I:C, effectively cause tumor cell death in colon carcinoma HCT116 cells.

We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.

On the other hand, IFN-alpha increased poly I:C-induced apoptosis and the TLR3 mRNA level in HCT116 p53(+/+) and p53(-/-) cell lines.

Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.

Considering that the p53 status in malignant cells is heterogeneous, this combination approach may provide a highly effective tumor therapy.

[MeSH-minor] Adenocarcinoma / genetics. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line. Cell Line, Tumor. Colorectal Neoplasms / genetics. DNA Damage / drug effects. Fluorouracil / pharmacology. Humans. Interferon-alpha / pharmacology. Interferon-beta / pharmacology. Kidney. Lung Neoplasms / genetics. Mice

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(PMID = 20367642.001).

[ISSN] 1349-7006

[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 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; U3P01618RT / Fluorouracil

   

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[Title] Tumor necrosis factor-{alpha} rs361525 polymorphism is associated with increased local production and downstream inflammation in chronic obstructive pulmonary disease.

RATIONALE: Chronic obstructive pulmonary disease (COPD) has a genetic component, explaining susceptibility.

Tumor necrosis factor (TNF)-alpha polymorphisms have been associated with COPD, but it is unclear if genotype influences clinical phenotype, protein expression, and bioactivity.

OBJECTIVES: To determine if a functional polymorphism was important by assessing TNF-alpha expression and activity and its association with clinical severity over time.

TNF-alpha, its antagonists, and downstream mediators were measured in plasma and sputum.

To determine TNF-alpha bioactivity, IL-8 secretion from primary bronchial epithelial cells (PBECs) was measured, and neutrophil migration was assessed using sputum from both subject groups in the presence and absence of TNF-alpha antibody.

MEASUREMENTS AND MAIN RESULTS: Patients with polymorphism had more chronic bronchitis, a lower body mass index, and a greater annual decline in FEV(1) than patients with COPD without rs361525 polymorphism.

TNF-alpha concentrations were 100-fold higher in airway secretions from the patients with the rs361525 polymorphism, with no difference in TNF-alpha antagonists.

These effects could be abrogated by TNF-alpha antibody, demonstrating the bioactivity of TNF-alpha in lung secretions from this group.

CONCLUSIONS: This TNF-alpha polymorphism is associated with clinical features of disease including progression.

There is clear evidence of TNF-alpha overexpression and bioactivity with neutrophilic inflammation.

The polymorphism is likely to be a factor that influences a COPD disease phenotype and its progression.

[MeSH-major] Polymorphism, Genetic. Pulmonary Disease, Chronic Obstructive / genetics. Tumor Necrosis Factor-alpha / genetics

[MeSH-minor] Adult. Aged. Body Mass Index. Bronchi / cytology. Bronchitis / epidemiology. Case-Control Studies. Cell Movement. Disease Progression. Epithelial Cells / metabolism. Female. Forced Expiratory Volume. Genotype. Humans. Interleukin-8 / metabolism. Interleukin-8 / secretion. Male. Middle Aged. Neutrophils / physiology. Peroxidase / metabolism. Phenotype. Severity of Illness Index. Sputum / metabolism

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(PMID = 20299531.001).

[ISSN] 1535-4970

[Journal-full-title] American journal of respiratory and critical care medicine

[ISO-abbreviation] Am. J. Respir. Crit. Care Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase

   

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[Title] Sphingosine-1-phosphate prevents tumor necrosis factor-{alpha}-mediated monocyte adhesion to aortic endothelium in mice.

Sphingosine-1-phosphate (S1P) is a sphingolipid that binds to G protein-coupled receptors on endothelial cells (ECs).

METHODS AND RESULTS: We injected C57BL/6J mice intravenously with tumor necrosis factor (TNF)-alpha in the presence and absence of the S1P1 receptor agonist SEW2871 and examined monocyte adhesion.

Aortas from TNF-alpha-injected mice had a 4-fold increase in the number of monocytes bound, whereas aortas from TNF-alpha plus SEW2871-treated mice had few monocytes bound (P<0.0001).

Using siRNA, we found that inhibiting the S1P1 receptor in vascular ECs blocked the ability of S1P to prevent monocyte-EC interactions in response to TNF-alpha.

We examined signaling pathways downstream of S1P1 and found that 100 nM S1P increased phosphorylation of Akt and decreased activation of c-jun.

CONCLUSIONS: Thus, we provide the first evidence that S1P signaling through the endothelial S1P1 receptor protects the vasculature against TNF-alpha-mediated monocyte-EC interactions in vivo.

[MeSH-major] Cell Adhesion / drug effects. Endothelium, Vascular / cytology. Lysophospholipids / pharmacology. Monocytes / cytology. Sphingosine / analogs & derivatives. Tumor Necrosis Factor-alpha / metabolism. Vasculitis / drug therapy

[MeSH-minor] Animals. Aorta / cytology. Aorta / immunology. Cells, Cultured. Chemokines / metabolism. E-Selectin / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Mice. Mice, Inbred C57BL. Oxadiazoles / pharmacology. Receptors, Lysosphingolipid / agonists. Receptors, Lysosphingolipid / metabolism. Signal Transduction / drug effects. Signal Transduction / immunology. Thiophenes / pharmacology. Vascular Cell Adhesion Molecule-1 / metabolism

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(PMID = 15761190.001).

[ISSN] 1524-4636

[Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology

[ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / F31 GM064101; United States / NIGMS NIH HHS / GM / R01 GM067958; United States / NHLBI NIH HHS / HL / R01 HL079621

[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 / Chemokines; 0 / E-Selectin; 0 / Lysophospholipids; 0 / Oxadiazoles; 0 / Receptors, Lysosphingolipid; 0 / SEW2871; 0 / Thiophenes; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 26993-30-6 / sphingosine 1-phosphate; NGZ37HRE42 / Sphingosine

   

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[Title] Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression.

T cells can inhibit tumor growth, but their function in the tumor microenvironment is often suppressed.

Many solid tumors exhibit abundant macrophage infiltration and low oxygen tension, yet how hypoxic conditions may affect innate immune cells and their role in tumor progression is poorly understood.

Targeted deletion of the hypoxia-responsive transcription factor hypoxia-inducible factor-1α (HIF-1α) in macrophages in a progressive murine model of breast cancer resulted in reduced tumor growth, although vascular endothelial growth factor-A levels and vascularization were unchanged.

Tumor-associated macrophages can suppress tumor-infiltrating T cells by several mechanisms, and we found that hypoxia powerfully augmented macrophage-mediated T-cell suppression in vitro in a manner dependent on macrophage expression of HIF-1α.

Our findings link the innate immune hypoxic response to tumor progression through induction of T-cell suppression in the tumor microenvironment.

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[Copyright] © 2010 AACR.

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(PMID = 20841473.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA118165; United States / NCI NIH HHS / CA / R01 CA082515; United States / NCI NIH HHS / CA / R01 CA130980; United States / NIAID NIH HHS / AI / R01 AI072117; United States / NCI NIH HHS / CA / R01 CA118165; United States / NCI NIH HHS / CA / R01 CA130980-03

[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 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse

[Other-IDs] NLM/ NIHMS226663; NLM/ PMC2948598

   

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[Title] Recombinant alpha-fetoprotein C-terminal fragment: the new recombinant vector for targeted delivery.

The specific receptor of alpha-fetoprotein (AFP) is a universal tumor marker, being expressed on the surface of many tumor cells, but not in normal human tissues.

AFP enters the cell by receptor-mediated endocytosis; its receptor-binding site is hypothetically localized in the third domain of AFP.

A recombinant C-terminal AFP fragment, which contains all the third and a part of the second domains of hAFP, was produced.

This AFP fragment was bound specifically to the AFP receptor on the surface of tumor cells and was accumulated by them with the same efficiency as the full-size hAFP.

Similar to hAFP, the recombinant C-terminal fragment inhibited the estradiol-induced growth of hormone-dependent MCF-7 cells in vitro.

Hence, the recombinant C-terminal AFP fragment can be used as a protein vector for the targeted delivery of cytostatic drugs to tumor cells.

[MeSH-major] Drug Carriers / pharmacology. alpha-Fetoproteins / pharmacology

[MeSH-minor] Antineoplastic Agents / administration & dosage. Bacteria / drug effects. Bacteria / genetics. Cell Line, Tumor. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Escherichia coli / metabolism. Estradiol / pharmacology. Female. Fluorescein-5-isothiocyanate. Fluorescent Dyes. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Microscopy, Fluorescence. Protein Folding. Receptors, Peptide / metabolism. Recombinant Proteins / pharmacology

Hazardous Substances Data Bank. ESTRADIOL .

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(PMID = 18446611.001).

[ISSN] 1061-186X

[Journal-full-title] Journal of drug targeting

[ISO-abbreviation] J Drug Target

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Complementary; 0 / Drug Carriers; 0 / Fluorescent Dyes; 0 / Receptors, Peptide; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins; 0 / alpha-fetoprotein receptor, human; 4TI98Z838E / Estradiol; I223NX31W9 / Fluorescein-5-isothiocyanate

   

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[Title] Antitumor activities of O-sulfonated derivatives of (1-->3)-alpha-D-glucan from different Lentinus edodes.

Four water-insoluble (1-->3)-alpha-D-glucans, coded L-II1, L-II2, L-II3 and L-II4, with different molecular weights were isolated from four kinds of fruiting bodies of Lentinus Edodes.

The four alpha-D-glucans were O-sulfonated to obtain derivatives (SL-II) having degrees of substitution (DS) from 0.9 to 2.1 respectively.

The structure of the samples was analyzed by infrared spectra, elemental analysis, and 13C NMR.

The weight-average molecular weight (Mw), radii of gyration (<s2>z1/2) and intrinsic viscosity ([eta]) of the native alpha-D-glucans and O-sulfonated derivatives were measured by size-exclusion chromatography combined with laser light scattering (SEC-LLS), LLS, and viscometry in 0.2 M aqueous NaCl and in dimethyl sulfoxide (DMSO) containing 0.25 M LiCl at 25 degrees C respectively.

The Mw values of the O-sulfonated derivatives were much lower than those of the native alpha-D-glucans.

The experimental results indicate that the O-sulfonated derivatives are water-soluble and exist as an expanded flexible chain in aqueous solution owing to intramolecular hydrogen bonding or interaction between charge groups.

The in vivo and in vitro antitumor activities of the native alpha-D-glucans and their O-sulfonated derivatives against solid tumor Sarcoma 180 cells were evaluated and compared.

The results reveal that the effect of O-sulfonation of the alpha-D-glucan on the improvement of their antitumor activities was considerable.

[MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred BALB C. Molecular Weight. Spectroscopy, Fourier Transform Infrared. Viscosity

Hazardous Substances Data Bank. Sulfur, Elemental .

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(PMID = 16428819.001).

[ISSN] 0916-8451

[Journal-full-title] Bioscience, biotechnology, and biochemistry

[ISO-abbreviation] Biosci. Biotechnol. Biochem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucans; 70FD1KFU70 / Sulfur; 9051-95-0 / alpha-1,3-glucan

   

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[Title] Endotoxin-independent white cell cytokine production in haemodynamically stable patients with idiopathic dilated cardiomyopathy.

INTRODUCTION: In heart failure, increased circulating white cell tumour necrosis factor-alpha production could be attributed to elevated plasma endotoxin concentrations or an increase in white cell sensitivity to endotoxin.

AIMS: To ascertain whether, in patients with IDC, circulating white cell TNF-alpha production is also mediated through endotoxin-independent mechanisms.

METHODS: Whole blood production of TNF-alpha, both with and without the presence of an endotoxin stimulus, was evaluated in 89 controls and in 60 patients with IDC in New York Heart Association functional class I, II or III heart failure and without evidence of oedema, reduced peripheral perfusion or elevated plasma endotoxin concentrations.

RESULTS: In patients compared to controls, IgG (p < 0.01) (IgG1 and IgG3), but not IgM concentrations were elevated, and plasma TNF-alpha and TGF-beta concentrations were raised (p < 0.001, p < 0.02 respectively).

In addition, endotoxin-free cultured whole blood TNF-alpha production (p < 0.0005) was increased.

Against a role for endotoxin-mediated pre-activation of white cells in patients, the sensitivity of white cells to endotoxin, as determined from the excitatory endotoxin concentration producing 50% maximal TNF-alpha production was unchanged.

Moreover, in favour of non-endotoxin-mediated white cell activation, the calcineurin inhibitor, cyclosporin-A, which did not alter endotoxin-induced TNF-alpha production, decreased TNF-alpha produced by unstimulated cultured cells in patients to values not significantly greater than those in controls.

CONCLUSIONS: We concluded that circulating white cell cytokine over-production can occur through both endotoxin- dependent and -independent mechanisms in IDC.

[MeSH-major] Cardiomyopathy, Dilated / blood. Endotoxins / pharmacology. Leukocytes / metabolism. Tumor Necrosis Factor-alpha / biosynthesis

[MeSH-minor] Female. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. In Vitro Techniques. Lymphotoxin-alpha / blood. Male. Middle Aged

Genetic Alliance. consumer health - Cardiomyopathy.

Genetic Alliance. consumer health - Dilated Cardiomyopathy.

Genetic Alliance. consumer health - Idiopathic dilated cardiomyopathy.

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(PMID = 16307158.001).

[Journal-full-title] Cardiovascular journal of South Africa : official journal for Southern Africa Cardiac Society [and] South African Society of Cardiac Practitioners

[ISO-abbreviation] Cardiovasc J S Afr

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] South Africa

[Chemical-registry-number] 0 / Endotoxins; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Inhibition of tumor necrosis factor-alpha-inducible inflammatory genes by interferon-gamma is associated with altered nuclear factor-kappaB transactivation and enhanced histone deacetylase activity.

Airway smooth muscle (ASM) cells can act as effector cells in the initiation and/or perpetuation of airway inflammation in asthma by producing various inflammatory chemokines or cytokines.

Previous studies from our laboratory and others showed that the combination of tumor necrosis factor-alpha (TNFalpha) and interferon-gamma (IFNgamma) or endogenous IFNbeta results in a synergistic induction of various pro-inflammatory genes, including CD38 and regulated upon activation normal T-cell expressed and secreted (RANTES), in ASM cells.

[MeSH-major] Gene Expression Regulation / drug effects. Histone Deacetylases / metabolism. Inflammation / genetics. Interferon-gamma / pharmacology. NF-kappa B / genetics. Tumor Necrosis Factor-alpha / pharmacology

[MeSH-minor] Cells, Cultured. Chemokine CCL11. Chemokines, CC / biosynthesis. Dose-Response Relationship, Drug. Drug Synergism. Humans. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Myocytes, Smooth Muscle / cytology. Trachea / cytology. Transcriptional Activation

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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(PMID = 17108260.001).

[ISSN] 0026-895X

[Journal-full-title] Molecular pharmacology

[ISO-abbreviation] Mol. Pharmacol.

[Language] eng

[Grant] United States / NHLBI NIH HHS / HL / HL064063

[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 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Chemokines, CC; 0 / Interleukin-6; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.5.1.98 / Histone Deacetylases