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1. Lepique AP, Forti FL, Moraes MS, Armelin HA: Signal transduction in G0/G1-arrested mouse Y1 adrenocortical cells stimulated by ACTH and FGF2. Endocr Res; 2000 Nov;26(4):825-32
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  • [Title] Signal transduction in G0/G1-arrested mouse Y1 adrenocortical cells stimulated by ACTH and FGF2.
  • In G0/G1 cell cycle arrested mouse Y1 adrenocortical tumor cells ACTH39, a weak mitogen and strong anti-mitogenic agent, blocks FGF2 mitogenic activity at G1 phase, keeping untouched ERK-MAPK activation and c-Fos protein induction.
  • Here we report two anti-mitogenic mechanisms initiated in ACTH receptors and mediated by cAMP/PKA: a) post-transcriptional down regulation of c-Myc protein;.
  • ACTH39, on the other hand, causes rapid decrease in c-Myc levels induced by FGF2 in wild type Y1 cells, but not in PKA-deficient Y1 clones.
  • The ACTH inhibition of DNA synthesis stimulated by FGF2 is reversed by transient transfection and induction of the MycER chimera (fusion of c-Myc and estrogen-receptor), suggesting that c-Myc down regulation is an efficient anti-mitogenic mechanism activated by ACTH.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenocorticotropic Hormone / pharmacology. Fibroblast Growth Factor 2 / pharmacology. G0 Phase / physiology. G1 Phase / physiology. Protein-Serine-Threonine Kinases. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Down-Regulation. Mice. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Proto-Oncogene Proteins c-myc / metabolism. Tumor Cells, Cultured

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  • (PMID = 11196459.001).
  • [ISSN] 0743-5800
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 103107-01-3 / Fibroblast Growth Factor 2; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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2. Kempná P, Körner M, Waser B, Hofer G, Nuoffer JM, Reubi JC, Flück CE: Neuropeptide Y modulates steroid production of human adrenal H295R cells through Y1 receptors. Mol Cell Endocrinol; 2010 Jan 15;314(1):101-9
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  • [Title] Neuropeptide Y modulates steroid production of human adrenal H295R cells through Y1 receptors.
  • The human adrenal cortex and adrenal tumors express NPY receptor subtype Y1, but its function is unknown.
  • We studied Y1-mediated signaling, steroidogenesis and cell proliferation in human adrenal NCI-H295R cells.
  • Studies of the effect of NPY and related peptide PYY on adrenal steroidogenesis revealed a decrease in 11-deoxycortisol production.
  • RIA measurements of cortisol from cell culture medium confirmed this finding.
  • Our data show that NPY can directly regulate human adrenal cortisol production.
  • [MeSH-major] Adrenal Glands / cytology. Neuropeptide Y / metabolism. Receptors, Neuropeptide Y / metabolism
  • [MeSH-minor] Aldosterone / biosynthesis. Cell Line. Cell Proliferation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Hydrocortisone / biosynthesis. Hydroxysteroid Dehydrogenases / genetics. Hydroxysteroid Dehydrogenases / metabolism. MAP Kinase Kinase Kinases / metabolism. Peptide YY / metabolism. Radioimmunoassay. Signal Transduction / physiology. Testosterone / biosynthesis

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  • (PMID = 19699258.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Neuropeptide Y; 0 / Receptors, Neuropeptide Y; 0 / neuropeptide Y-Y1 receptor; 106388-42-5 / Peptide YY; 3XMK78S47O / Testosterone; 4964P6T9RB / Aldosterone; EC 1.1.- / Hydroxysteroid Dehydrogenases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; WI4X0X7BPJ / Hydrocortisone
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3. Komorowski J, Jurczynska J, Stepien T, Kolomecki K, Kuzdak K, Stepien H: Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery. Int J Mol Sci; 2010;11(6):2281-90
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  • [Title] Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery.
  • The peripheral blood levels of TNF alpha and its soluble receptors were studied in 39 patients with malignant and benign adrenal tumors treated by adrenalectomy.
  • The concentrations of TNF alpha were significantly elevated in patients with malignant tumors of the adrenal cortex and in patients with Conn's syndrome compared to control.
  • After adrenalectomy, the levels of TNF alpha were decreased in patients with malignant tumors and in patients with Conn's syndrome, nonfunctioniong adenomas and pheochromocytomas compared to the concentration before surgery.
  • However, to confirm practicality of the evaluation of TNF alpha and its soluble receptors in differential diagnosis in patients with adrenal tumors, a larger study group is needed.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / surgery. Receptors, Tumor Necrosis Factor / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adrenalectomy. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Receptors, Tumor Necrosis Factor, Type I / blood. Receptors, Tumor Necrosis Factor, Type II / blood

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  • (PMID = 20640152.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2904916
  • [Keywords] NOTNLM ; TNF α / TNF α R1 / TNF α R2 / adrenal tumors / adrenalectomy
  • [General-notes] NLM/ Original DateCompleted: 20110714
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4. Nogueira EF, Vargas CA, Otis M, Gallo-Payet N, Bollag WB, Rainey WE: Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells. J Mol Endocrinol; 2007 Dec;39(6):365-74
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  • [Title] Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells.
  • Angiotensin-II (Ang-II) regulates adrenal steroid production and gene transcription through several signaling pathways.
  • Microarray analyses were performed using samples from control and Ang-II (10 nM)-treated (1 h) cells from human adrenocortical tumor cell line H295R, and primary adrenal glomerulosa cells from bovine and rat, applied respectively to human, bovine, and rat chips. qPCR was performed to confirm up-regulation of selected genes using mRNA.
  • The Ang-II gene targets have been defined in three different adrenocortical model systems.
  • Several of the listed genes have previously been described as being key regulators of adrenocortical function.
  • The presence of adrenal cell common genes in such distinct cell models strengthens the hypothesis that these genes are regulators of aldosterone production.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / drug effects. Angiotensin II / pharmacology. Gene Expression Regulation / drug effects
  • [MeSH-minor] Animals. Cattle. Cell Line, Tumor. Female. Humans. Male. Microarray Analysis. Rats. Species Specificity. Zona Glomerulosa / cytology. Zona Glomerulosa / drug effects. Zona Glomerulosa / metabolism

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  • (PMID = 18055484.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE8442
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140; United States / NHLBI NIH HHS / HL / HL70046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 11128-99-7 / Angiotensin II
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5. Lotfi CF, Costa ET, Schwindt TT, Armelin HA: Role of ERK/MAP kinase in mitogenic interaction between ACTH and FGF2 in mouse Y1 adrenocortical tumor cells. Endocr Res; 2000 Nov;26(4):873-7
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  • [Title] Role of ERK/MAP kinase in mitogenic interaction between ACTH and FGF2 in mouse Y1 adrenocortical tumor cells.
  • In G0/G1 cell cycle-arrested Y1 adrenocortical cells FGF2 is a strong mitogen, whereas ACTH39 can be a weak mitogen or a strong anti-mitogenic agent.
  • Phosphorylated ERK1/2-MAP kinases are undetectable by Western and immunocitochemistry assay in G0/G1-arrested Y1 adrenal cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocorticotropic Hormone / pharmacology. Fibroblast Growth Factor 2 / pharmacology. Mitogen-Activated Protein Kinases / physiology. Mitogens / pharmacology
  • [MeSH-minor] Animals. Cyclin D1 / metabolism. DNA / biosynthesis. Dose-Response Relationship, Drug. Drug Interactions. Mice. Phosphorylation. Proto-Oncogene Proteins c-fos / metabolism


6. Schwindt TT, Forti FL, Juliano MA, Juliano L, Armelin HA: Arginine vasopressin inhibition of cyclin D1 gene expression blocks the cell cycle and cell proliferation in the mouse Y1 adrenocortical tumor cell line. Biochemistry; 2003 Feb 25;42(7):2116-21
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  • [Title] Arginine vasopressin inhibition of cyclin D1 gene expression blocks the cell cycle and cell proliferation in the mouse Y1 adrenocortical tumor cell line.
  • In G0/G1-arrested mouse Y1 adrenocortical tumor cells, maintained in serum-free medium (SFM), AVP mimics FGF2, promoting rapid ERK1/2 activation (5 min) followed by c-Fos protein induction (2 h).
  • AVP inhibition of cyclin D1 expression is sufficient to block G1 phase progression and cell entry into the S phase, monitored by BrdU nuclear labeling.
  • On the other hand, ectopic expression of the cyclin D1 protein renders Y1 cells resistant to AVP for both entry into the S phase in SFM and continuous proliferation in 10% FCS medium.
  • In conclusion, inhibition of cyclin D1 expression by AVP is an efficient mechanism of cell cycle blockage and consequent proliferation inhibition in Y1 adrenocortical cells.
  • [MeSH-major] Arginine Vasopressin / physiology. Cell Cycle / physiology. Cyclin D1 / antagonists & inhibitors. Cyclin D1 / biosynthesis. Gene Expression Regulation / physiology. Growth Inhibitors / physiology. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / pathology
  • [MeSH-minor] Adrenal Cortex Neoplasms / enzymology. Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Animals. Clone Cells. Culture Media, Conditioned. Drug Resistance, Neoplasm. Enzyme Activators / pharmacology. Fibroblast Growth Factor 2 / pharmacology. G0 Phase / drug effects. G0 Phase / physiology. G1 Phase / drug effects. G1 Phase / physiology. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Molecular Mimicry. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase C / physiology. Transfection

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  • (PMID = 12590600.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Enzyme Activators; 0 / Growth Inhibitors; 103107-01-3 / Fibroblast Growth Factor 2; 113-79-1 / Arginine Vasopressin; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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7. Boulle N, Gicquel C, Logié A, Christol R, Feige JJ, Le Bouc Y: Fibroblast growth factor-2 inhibits the maturation of pro-insulin-like growth factor-II (Pro-IGF-II) and the expression of insulin-like growth factor binding protein-2 (IGFBP-2) in the human adrenocortical tumor cell line NCI-H295R. Endocrinology; 2000 Sep;141(9):3127-36
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  • [Title] Fibroblast growth factor-2 inhibits the maturation of pro-insulin-like growth factor-II (Pro-IGF-II) and the expression of insulin-like growth factor binding protein-2 (IGFBP-2) in the human adrenocortical tumor cell line NCI-H295R.
  • The IGF system is thought to play a major role in adrenocortical tumorigenesis.
  • In this study, we used the NCI H295R cell line as a model to investigate the effects of fibroblast growth factor-2 (FGF-2), a potent mitogen for normal adrenal cells, on the proliferation and on the expression of the IGF system in cultured adrenocortical tumor cells.
  • Recombinant human FGF-2 stimulated the proliferation of adrenocortical tumor cells in a dose- and time-dependent manner, with a maximal effect at a concentration of about 1 ng/ml.
  • Altogether, these results indicate that FGF-2 is mitogenic for NCI H295R tumor cells and regulates the expression of both IGF-II and IGFBP-2 in this tumor model.
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Blotting, Northern. Blotting, Western. Cell Division / drug effects. Cell Line. Densitometry. Electrophoresis, Polyacrylamide Gel. Humans. Mitogens / pharmacology. RNA / biosynthesis. Thymidine / metabolism. Tumor Cells, Cultured

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  • (PMID = 10965883.001).
  • [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 / Insulin-Like Growth Factor Binding Protein 2; 0 / Mitogens; 0 / Protein Precursors; 0 / proinsulin-like growth factor II; 103107-01-3 / Fibroblast Growth Factor 2; 63231-63-0 / RNA; 67763-97-7 / Insulin-Like Growth Factor II; VC2W18DGKR / Thymidine
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8. Forti FL, Costa ET, Rocha KM, Moraes MS, Armelin HA: c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line. An Acad Bras Cienc; 2006 Jun;78(2):231-9
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  • [Title] c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line.
  • The mouse Y1 adrenocortical tumor cell line is highly responsive to FGF2-(Fibroblast Growth Factor 2) and possesses amplified and over-expressed c-Ki-ras proto-oncogene.
  • On the other hand, activation levels of another important pathway downstream of c-Ki-Ras-GTP, namely, Raf-->MEK-->ERK, remain strictly dependent on FGF2 stimulation (Rocha et al. 2003).
  • Here we show that, first, FGF2 transiently up-regulates the c-Ki-Ras-GTP-->PI3K-->Akt pathway, in spite of its high basal levels.
  • But, Y1 cells, expressing dominant negative mutant RasN17, display a rapid and transient up-regulation of c-H-Ras-GTP upon FGF2 treatment.
  • Elucidation of FGF2-signaling pathways in Y1 tumor cells can uncover new targets for drug development of interest in cancer therapy.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Fibroblast Growth Factor 2 / genetics. Genes, ras / genetics. Signal Transduction / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Transformation, Neoplastic. Gene Amplification. Gene Expression Regulation, Neoplastic. Mice


9. Fassnacht M, Hahner S, Hansen IA, Kreutzberger T, Zink M, Adermann K, Jakob F, Troppmair J, Allolio B: N-terminal proopiomelanocortin acts as a mitogen in adrenocortical tumor cells and decreases adrenal steroidogenesis. J Clin Endocrinol Metab; 2003 May;88(5):2171-9
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  • [Title] N-terminal proopiomelanocortin acts as a mitogen in adrenocortical tumor cells and decreases adrenal steroidogenesis.
  • There is evidence that proopiomelanocortin (POMC)-derived peptides other than ACTH are involved in pituitary-dependent adrenal growth.
  • We have synthesized the human N-terminal POMC fragment 1-28-POMC with the disulfide bridges in the correct position between cysteine residues 2-24 and 8-20 and studied the activity of these peptides in adrenocortical tumor cells in vitro.
  • 1-28-POMC stimulated cell proliferation in human NCI-h295 and mouse Y-1 adrenal cancer cell lines and also in primary cultures of bovine adrenocortical cells in a concentration-dependent manner.
  • However, protein levels of important regulators of steroidogenesis [steroidogenic factor-1, DAX-1 (dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X-chromosome 1), steroidogenic acute regulatory protein, and cytochrome P450 side-chain cleavage enzyme] remained unaffected by 1-28-POMC treatment.
  • Our results provide evidence that synthetic 1-28-POMC induces adrenal tumor cell proliferation, inhibits adrenal steroidogenesis, and mediates its action by signaling via the extracellular signal-regulated kinase pathway.
  • The distinct roles of 1-28-POMC and ACTH in the regulation of adrenal growth and steroidogenesis suggest that the adrenal cortex is under the dual opposing control of fragments from the same mother peptide POMC.
  • [MeSH-major] Adrenal Cortex Hormones / biosynthesis. Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Mitogens / pharmacology. Peptide Fragments / pharmacology. Pro-Opiomelanocortin / pharmacology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Adrenal Cortex / drug effects. Animals. Cattle. Cell Division / drug effects. Cells, Cultured. Dehydroepiandrosterone Sulfate / metabolism. Enzyme Activation / drug effects. Humans. Hydrocortisone / biosynthesis. JNK Mitogen-Activated Protein Kinases. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Signal Transduction. Tumor Cells, Cultured. p38 Mitogen-Activated Protein Kinases

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  • (PMID = 12727972.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Mitogens; 0 / Peptide Fragments; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 66796-54-1 / Pro-Opiomelanocortin; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; WI4X0X7BPJ / Hydrocortisone
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10. Doghman M, Karpova T, Rodrigues GA, Arhatte M, De Moura J, Cavalli LR, Virolle V, Barbry P, Zambetti GP, Figueiredo BC, Heckert LL, Lalli E: Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer. Mol Endocrinol; 2007 Dec;21(12):2968-87
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  • [Title] Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer.
  • Steroidogenic factor-1 (SF-1/Ad4BP; NR5A1), a nuclear receptor transcription factor, has a pivotal role in adrenal and gonadal development in humans and mice.
  • A frequent feature of childhood adrenocortical tumors is SF-1 amplification and overexpression.
  • Here we show that an increased SF-1 dosage can by itself augment human adrenocortical cell proliferation through concerted actions on the cell cycle and apoptosis.
  • Consistent with these results, increased SF-1 levels selectively modulate the steroid secretion profile of adrenocortical cells, reducing cortisol and aldosterone production and maintaining dehydroepiandrosterone sulfate secretion.
  • As a model to understand the mechanisms of transcriptional regulation by increased SF-1 dosage, we studied FATE1, coding for a cancer-testis antigen implicated in the control of cell proliferation.
  • On the other hand, sphingosine, which can compete with phospholipids for binding to SF-1, had no effect on the SF-1 dosage-dependent increase of adrenocortical cell proliferation and expression of the FATE1 promoter.
  • In mice, increased Sf-1 dosage produces adrenocortical hyperplasia and formation of tumors expressing gonadal markers (Amh, Gata-4), which originate from the subcapsular region of the adrenal cortex.
  • Gene expression profiling revealed that genes involved in cell adhesion and the immune response and transcription factor signal transducer and activator of transcription-3 (Stat3) are differentially expressed in Sf-1 transgenic mouse adrenals compared with wild-type adrenals.
  • Our studies reveal a critical role for SF-1 dosage in adrenocortical tumorigenesis and constitute a rationale for the development of drugs targeting SF-1 transcriptional activity for adrenocortical tumor therapy.

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  • (PMID = 17761949.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE5911/ GSE5912
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD038498; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907; United States / NICHD NIH HHS / HD / U54-HD28934
  • [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 / STAT3 Transcription Factor; 0 / Steroidogenic Factor 1; 0 / Steroids; 4QD397987E / Histidine
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11. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • [Title] Genetics of adrenal tumors.
  • The impact of genetics and genomics on clinical medicine is becoming more and more important.
  • Endocrinology pioneered the development of molecular medicine, but also the study of adrenal tumors had a great impact in this field.
  • Particularly important was the detection of genetics of tumors derived from the adrenal medulla, as well as that of those derived from the sympathetic and parasympathetic paraganglia.
  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • There are only a few examples of hereditary transmission of adrenocortical carcinoma, but the analysis of low penetrance genes by genome wide association study may enable us to discover new genetic mechanisms responsible for adrenocortical-derived tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Mutation. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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12. Voets M, Müller-Vieira U, Marchais-Oberwinkler S, Hartmann RW: Synthesis of amidinohydrazones and evaluation of their inhibitory effect towards aldosterone synthase (CYP11B2) and the formation of selected steroids. Arch Pharm (Weinheim); 2004 Jul;337(7):411-6
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  • The synthesis and biological evaluation of a series of amidinohydrazones (3a-h, 6a-c, 8 and 9) as potential nonsteroidal inhibitors of aldosterone synthase (CYP11B2) are described.
  • Compound 6c was evaluated for its effect on the formation of aldosterone, cortisol, androstenedione, and DHEA in the adrenocortical tumor cell line NCI-H295R.
  • It exhibited no significant effect on the production of these products.
  • [MeSH-minor] Aldosterone / biosynthesis. Androstenedione / biosynthesis. Cell Line, Tumor. Dehydroepiandrosterone / biosynthesis. Drug Design. Humans. Hydrocortisone / biosynthesis. Schizosaccharomyces / drug effects. Schizosaccharomyces / enzymology

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  • (PMID = 15237392.001).
  • [ISSN] 0365-6233
  • [Journal-full-title] Archiv der Pharmazie
  • [ISO-abbreviation] Arch. Pharm. (Weinheim)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Amidines; 0 / Hydrazones; 0 / Steroids; 409J2J96VR / Androstenedione; 459AG36T1B / Dehydroepiandrosterone; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; WI4X0X7BPJ / Hydrocortisone
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13. Pereira RM, Michalkiewicz E, Pianovski MA, França SN, Boguszewski MC, Cat I, Lacerda Filho Ld, Sandrini R: [Treatment of childhood adrenocortical tumor]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):747-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of childhood adrenocortical tumor].
  • [Transliterated title] Tratamento do tumor do córtex adrenal na infância.
  • Adrenocortical tumors (ACT) in children are uncommon.
  • However, the incidence of these tumors in Paraná is 15 times higher than that worldwide.
  • In our experience, disease stage I, absence of spillage during surgery and absence of intravenous thrombus are associated with better survival rates.
  • Preliminary data with the combination of etoposide, doxorubicin, cisplatin, and mitotane have shown that in some patients a complete remission is observed both of the tumor and metastasis.
  • Side effects due to these drugs are common and adrenal insufficiency may occur.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Carcinoma
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Infant. Male. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 16444357.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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14. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • In addition, since RGZ can reduce ACTH and corticosterone secretion in mouse corticotropic pituitary tumors, both RGZ and PIO have been used in the treatment of Cushing's disease with variable but generally unsatisfactory results.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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15. Fon WP, Li PH: Dexamethasone-induced suppression of steroidogenic acute regulatory protein gene expression in mouse Y-1 adrenocortical cells is associated with reduced histone H3 acetylation. Endocrine; 2007 Oct;32(2):155-65
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  • [Title] Dexamethasone-induced suppression of steroidogenic acute regulatory protein gene expression in mouse Y-1 adrenocortical cells is associated with reduced histone H3 acetylation.
  • In this study, we investigated the effect of dexamethasone on the expression of steroidogenic acute regulatory protein (StAR) and the acetylation of histone H3 in mouse Y-1 adrenocortical tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Dexamethasone / pharmacology. Glucocorticoids / pharmacology. Histones / metabolism. Phosphoproteins / metabolism
  • [MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Acetylation / drug effects. Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Mice. Progesterone / metabolism. Promoter Regions, Genetic / genetics. RNA, Messenger / metabolism. Receptors, Glucocorticoid / genetics. Receptors, Glucocorticoid / metabolism

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  • (PMID = 18040891.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Histones; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Receptors, Glucocorticoid; 0 / steroidogenic acute regulatory protein; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 4G7DS2Q64Y / Progesterone; 7S5I7G3JQL / Dexamethasone
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16. Forti FL, Armelin HA: ACTH inhibits A Ras-dependent anti-apoptotic and mitogenic pathway in mouse Y1 adrenocortical cells. Endocr Res; 2000 Nov;26(4):911-4
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  • [Title] ACTH inhibits A Ras-dependent anti-apoptotic and mitogenic pathway in mouse Y1 adrenocortical cells.
  • Mouse Y1 adrenocortical tumor cells harbor amplified and overexpressed c-Ki-ras gene, displaying relatively high constitutive levels of Ras x GTP.
  • This ACTH inhibition of the anti-apoptic and mitogenic AKT/PKB pathway is likely to be relevant in ACTH growth inhibitory effects in Y-adrenocortical cells.
  • [MeSH-major] Adrenal Cortex / physiology. Adrenocorticotropic Hormone / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Mitogens / physiology. Protein-Serine-Threonine Kinases. Sulfonamides. ras Proteins / physiology
  • [MeSH-minor] Androstadienes / pharmacology. Animals. Cyclic AMP-Dependent Protein Kinases / physiology. Dexamethasone / pharmacology. Enzyme Inhibitors / pharmacology. Fibroblast Growth Factor 2 / pharmacology. Glucocorticoids / pharmacology. Isoquinolines / pharmacology. Mice. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Proto-Oncogene Proteins p21(ras) / physiology. Tumor Cells, Cultured

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  • (PMID = 11196470.001).
  • [ISSN] 0743-5800
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androstadienes; 0 / Enzyme Inhibitors; 0 / Glucocorticoids; 0 / Isoquinolines; 0 / Mitogens; 0 / Proto-Oncogene Proteins; 0 / Sulfonamides; 103107-01-3 / Fibroblast Growth Factor 2; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 3.6.5.2 / ras Proteins; XVA4O219QW / wortmannin
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17. Doghman M, Cazareth J, Lalli E: The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells. J Clin Endocrinol Metab; 2008 Aug;93(8):3222-5
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  • [Title] The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells.
  • CONTEXT: Mutations of the beta-catenin (CTNNB1) gene are frequently found in adrenocortical tumors.
  • OBJECTIVE: The objective of the study was to investigate the effect of the small-molecule inhibitor of the T cell factor (Tcf)/beta-catenin complex PKF115-584 on beta-catenin-dependent transcription and proliferation of H295R adrenocortical tumor cells, which harbor mutations in CTNNB1 as well as the TP53 tumor suppressor gene.
  • The drug had no effect on HeLa cells, a cell line in which the beta-catenin pathway is not activated.
  • CONCLUSIONS: Inhibitors of the Tcf/beta-catenin complex may prove useful in the treatment of adrenocortical tumors in which multiple genetic alterations have accumulated.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. TCF Transcription Factors / antagonists & inhibitors. beta Catenin / antagonists & inhibitors
  • [MeSH-minor] Cell Proliferation / drug effects. Genes, p53. Humans. Mutation. Tumor Cells, Cultured

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  • (PMID = 18544621.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TCF Transcription Factors; 0 / beta Catenin
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18. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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19. Sutter JA, Grimberg A: Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy. Pediatr Endocrinol Rev; 2006 Sep;4(1):32-9
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  • [Title] Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy.
  • Adrenocortical tumors are rare in children and are associated with a poor prognosis when malignant.
  • Evaluation of genetic disorders associated with the development of adrenocortical disorders has allowed researchers to identify a number of mutations that may be involved in tumorigenesis, including alterations in the GNAS1, PRKAR1A, TP53 and IGF2 genes.
  • Most children have localized disease at presentation which may be associated with a better prognosis when compared to adults.
  • Surgical resection remains the only potentially curative treatment and mitotane, the most frequently used chemotherapeutic agent, has a poor response rate and is highly toxic.
  • Broader participation in multi-center research, such as the International Pediatric Adrenocortical Tumor Registry, is needed to collect sufficient data to better guide our clinical management.

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  • (PMID = 17021581.001).
  • [ISSN] 1565-4753
  • [Journal-full-title] Pediatric endocrinology reviews : PER
  • [ISO-abbreviation] Pediatr Endocrinol Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064352; United States / NIDDK NIH HHS / DK / 5K08 DK64352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Israel
  • [Number-of-references] 73
  • [Other-IDs] NLM/ NIHMS22957; NLM/ PMC1907361
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20. Lin X, Takemori H, Katoh Y, Doi J, Horike N, Makino A, Nonaka Y, Okamoto M: Salt-inducible kinase is involved in the ACTH/cAMP-dependent protein kinase signaling in Y1 mouse adrenocortical tumor cells. Mol Endocrinol; 2001 Aug;15(8):1264-76
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  • [Title] Salt-inducible kinase is involved in the ACTH/cAMP-dependent protein kinase signaling in Y1 mouse adrenocortical tumor cells.
  • The involvement of salt-inducible kinase, a recently cloned protein serine/threonine kinase, in adrenal steroidogenesis was investigated.
  • When Y1 mouse adrenocortical tumor cells were stimulated by ACTH, the cellular content of salt-inducible kinase mRNA, protein, and enzyme activity changed rapidly.
  • These results suggested that salt-inducible kinase might play an important role(s) in the cAMP-dependent, but Ad4BP/steroidogenic factor-1-independent, gene expression of cholesterol side-chain cleavage cytochrome P450 in adrenocortical cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenocorticotropic Hormone / pharmacology. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Signal Transduction
  • [MeSH-minor] Adrenal Glands / enzymology. Animals. Cholesterol Side-Chain Cleavage Enzyme / genetics. Electrophoresis, Polyacrylamide Gel. Gene Expression / drug effects. Glutathione Transferase / genetics. Kinetics. Mice. Promoter Regions, Genetic. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Recombinant Fusion Proteins. Tissue Distribution. Transfection. Tumor Cells, Cultured

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  • (PMID = 11463852.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 9002-60-2 / Adrenocorticotropic Hormone; E0399OZS9N / Cyclic AMP; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Sik1 protein, rat; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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21. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • CONTEXT: Thiazolidinediones (TZDs) have been implemented into clinical practice for the treatment of type 2 diabetes mellitus as specific peroxisome proliferator-activated receptor (PPAR)-gamma ligands.
  • Moreover, recent evidence has suggested that TZDs might have favorable effects in the treatment of a variety of tumors as differentiation-inducing agents.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • Taken together, these data indicate that TZDs might have the potential to become an additional treatment option as differentiation-inducing agents in patients with ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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22. Forti FL, Dias MH, Armelin HA: ACTH receptor: ectopic expression, activity and signaling. Mol Cell Biochem; 2006 Dec;293(1-2):147-60
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  • Failure in obtaining expression of functional adrenocorticotropic hormone receptor (ACTHR, or melanocortin 2 receptor, MC2R) in non-adrenal cells has hindered molecular analysis of ACTH signaling pathways.
  • Natural constitutive expression of the MC2R accessory protein (MRAP) in Balb3T3 and other mouse 3T3 fibroblasts (NIH, Swiss and 3T3-L1) renders these fibroblastic lines suitable for ectopic expression of ACTHR in its active form properly inserted into the plasma membrane at levels similar to those found in mouse Y1 adrenocortical tumor cells.
  • The Y1 cell line is a cultured cell system well known for stably displaying normal adrenal specific metabolic pathways, ACTHR expression and ACTH functional responses.
  • Fourteen 3T3-AR and four 3T3-0 clones were screened for response to ACTH(39) in comparison with Y1 adrenocortical cells.
  • Eight 3T3-AR clones responded to ACTH(39) with activation of adenylate cyclase and induction of c-Fos protein, but the levels of, respectively, activation and induction were not strictly correlated.
  • In Y1 cells, specific inhibitors (H89/PKA; PD98059/MEK; Go6983/PKC and SP600125/JNK) show that signals initiated in the ACTH/ACTHR-system activate 4 pathways to induce the c-fos gene, namely: (a) cAMP/PKA/CREB;.
  • On the other hand, SP600125 caused 85% inhibition of c-Fos induction by ACTH(39) and, in addition, ACTH(39) promotes JNK1/2 phosphorylation, suggesting that JNK is a major signaling pathway mediating c-Fos induction by ACTH(39) in these cells.
  • However, activation of cAMP/PKA/CREB and JNK pathways and induction of fos and jun genes are not yet sufficient to enable ACTH for interference in morphology, migration and proliferation of Balb3T3 fibroblasts as it does in Y1 adrenocortical cells.
  • [MeSH-minor] 3T3 Cells. Adenylyl Cyclases / metabolism. Adrenal Cortex / metabolism. Adrenocorticotropic Hormone / metabolism. Animals. Cell Line, Tumor. Enzyme Activation. Fluorescent Antibody Technique. Gene Expression. Genes, fos. Genes, jun. Mice. Models, Biological. Phosphorylation. Transfection


23. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Bone morphogenetic proteins (BMP) have been shown to affect tumorigenesis in a variety of tumors.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 19584291.001).
  • [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 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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24. Costa ET, Forti FL, Rocha KM, Moraes MS, Armelin HA: Molecular mechanisms of cell cycle control in the mouse Y1 adrenal cell line. Endocr Res; 2004 Nov;30(4):503-9
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  • [Title] Molecular mechanisms of cell cycle control in the mouse Y1 adrenal cell line.
  • Y1 adrenocortical tumor cells possess amplified and overexpressed c-Ki-ras proto-oncogene, displaying chronic high levels of the c-Ki-Ras-GTP protein.
  • In effect, ACTH targets deactivation of constitutively phosphorylated-Akt, restraining the potential of c-Ki-Ras-GTP to subvert Y1 cell cycle control.
  • Thus, we can consider ACTH a tumor suppressor rather than an antimitogenic hormone.
  • In addition, we present initial results showing that high constitutive levels of c-Ki-Ras-GTP render Y1 cells susceptible to dye upon FGF2 treatment.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Glands / pathology. Cell Cycle
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Cell Line, Tumor. Cell Survival / drug effects. Fibroblast Growth Factor 2 / pharmacology. Mice. Mitosis / drug effects. Phosphorylation. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Proto-Oncogene Proteins p21(ras) / metabolism. Tumor Suppressor Proteins / pharmacology

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  • (PMID = 15666780.001).
  • [ISSN] 0743-5800
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 103107-01-3 / Fibroblast Growth Factor 2; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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25. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23
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  • Furthermore, SF-1 is amplified and overexpressed in most cases of adrenocortical tumor occurring in children; studies performed in transgenic mice have shown that an increased SF-1 dosage triggers tumor formation in the adrenal cortex.
  • For these reasons, drugs interfering with SF-1 action would represent a promising tool to be added to the current pharmacological protocols in the therapy of adrenocortical cancer.
  • These compounds have the attributes to inhibit the increase in proliferation triggered by an augmented SF-1 dosage in adrenocortical tumor cells and to reduce their steroid production.
  • This latter property may also reveal beneficial for drugs used in the therapy of adrenocortical tumors to alleviate symptoms of virilization and Cushing often associated with tumor burden.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21050908.001).
  • [ISSN] 1557-7988
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / U54 MH084512; United States / NIMH NIH HHS / MH / MH077624; United States / NIMH NIH HHS / MH / MH084512
  • [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 / Antineoplastic Agents; 0 / Isoquinolines; 0 / Steroidogenic Factor 1; 0 / Steroids
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26. Bey P, Gorostizaga AB, Maloberti PM, Lozano RC, Poderoso C, Cornejo Maciel F, Podestá EJ, Paz C: Adrenocorticotropin induces mitogen-activated protein kinase phosphatase 1 in Y1 mouse adrenocortical tumor cells. Endocrinology; 2003 Apr;144(4):1399-406
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  • [Title] Adrenocorticotropin induces mitogen-activated protein kinase phosphatase 1 in Y1 mouse adrenocortical tumor cells.
  • To determine whether MKP-1 is a component of ACTH cascade, here we investigate the expression levels of MKP-1 gene in Y1 mouse adrenocortical tumor cells under ACTH stimulation.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocorticotropic Hormone / pharmacology. Cell Cycle Proteins. Immediate-Early Proteins / genetics. Phosphoprotein Phosphatases. Protein Tyrosine Phosphatases / genetics. Sulfonamides
  • [MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Animals. Calcium Signaling / physiology. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cycloheximide / pharmacology. Dose-Response Relationship, Drug. Dual Specificity Phosphatase 1. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Isoquinolines / pharmacology. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Protein Phosphatase 1. Protein Synthesis Inhibitors / pharmacology. RNA, Messenger / analysis. Transcriptional Activation / drug effects. Tumor Cells, Cultured

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  • (PMID = 12639923.001).
  • [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 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Immediate-Early Proteins; 0 / Isoquinolines; 0 / Protein Synthesis Inhibitors; 0 / RNA, Messenger; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 9002-60-2 / Adrenocorticotropic Hormone; 98600C0908 / Cycloheximide; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / Dual Specificity Phosphatase 1; EC 3.1.3.48 / Dusp1 protein, mouse; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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27. Bassett MH, Zhang Y, White PC, Rainey WE: Regulation of human CYP11B2 and CYP11B1: comparing the role of the common CRE/Ad1 element. Endocr Res; 2000 Nov;26(4):941-51
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  • Reporter constructs prepared with the 5'flanking DNA of hCYP11B2 and hCYP11B1 were transfected into NCI-H295R (H295R) adrenocortical tumor cells.
  • Taken together these data suggest that the CRE/Adl element plays an important role in the transcriptional regulation of both hCYP11B genes but does not play an important role in the regional distribution of the two isozymes within the adrenal.
  • [MeSH-minor] Adrenal Glands / cytology. Adrenal Glands / physiology. Angiotensin II / pharmacology. Base Sequence / genetics. Cell Line. Gene Expression / drug effects. Genes, Reporter / drug effects. Genes, Reporter / physiology. Humans. Mutation / physiology. Potassium / pharmacology. Stereoisomerism. Transcription Factors / physiology. Transcription, Genetic / physiology. Transfection

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  • (PMID = 11196473.001).
  • [ISSN] 0743-5800
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK37867; United States / NIDDK NIH HHS / DK / DK43140
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors; 11128-99-7 / Angiotensin II; E0399OZS9N / Cyclic AMP; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; RWP5GA015D / Potassium
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28. Lichtenauer UD, Shapiro I, Geiger K, Quinkler M, Fassnacht M, Nitschke R, Rückauer KD, Beuschlein F: Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R. Endocrinology; 2008 Mar;149(3):1314-22
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  • [Title] Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R.
  • Recent evidence suggests the existence of a stem cell-like subpopulation of cells in hematological and solid tumor entities, which determine the malignant phenotype of a given tumor through their proliferative potential and chemotherapy resistance.
  • Herein we demonstrate the presence of SP cells in a variety of adrenal specimens, including primary cultures of human adrenocortical tumors and normal adrenal glands as well as established human and murine adrenocortical cancer cell lines by fluorescence-activated cell sorter analysis and confocal microscopy.
  • On a functional level, SP cells from the human adrenocortical tumor cell line NCI h295R revealed an expression pattern consistent with a less differentiated phenotype, including lower expression of steroidogenic enzymes such as steroid acute regulatory protein (StAR) and side-chain cleavage enzyme (P450scc) in comparison with non-SP cells.
  • Similarly to the baseline growth kinetics, no survival benefit was evident in SP cells after treatment with cytotoxic agents commonly used in adrenocortical carcinomas.
  • Taken together, these findings provide evidence that Hoechst dye exclusion, in contrast to what has been reported for other tumor entities, is not a major tumor stem cell defining marker in adrenocortical NCI h295R tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Adrenal Glands / cytology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / physiology. Cell Differentiation / physiology. Cell Line, Tumor. Cell Proliferation. Cholesterol Side-Chain Cleavage Enzyme / metabolism. Coloring Agents. Drug Resistance, Neoplasm / physiology. Humans. Phenotype. Phosphoproteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 18063677.001).
  • [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 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Phosphoproteins; 0 / steroidogenic acute regulatory protein; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme
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29. Katoh Y, Takemori H, Doi J, Okamoto M: Identification of the nuclear localization domain of salt-inducible kinase. Endocr Res; 2002 Nov;28(4):315-8
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  • Salt-inducible kinase (SIK), a novel serine/threonine protein kinase from adrenal glands of rats fed with a high-salt diet, is induced by ACTH in Y1 mouse adrenocortical tumor cells.
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Biological Transport / physiology. Cell Line. Cyclic AMP-Dependent Protein Kinases / metabolism. Cytosol / metabolism. Gene Expression / drug effects. Genes, Reporter / physiology. Mice. Phosphoproteins / genetics. Phosphorylation. Promoter Regions, Genetic / drug effects. Protein Structure, Tertiary / physiology. Rats. Time Factors. Tissue Distribution / drug effects. Tissue Distribution / physiology

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  • (PMID = 12530631.001).
  • [ISSN] 0743-5800
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphoproteins; 0 / steroidogenic acute regulatory protein; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Sik1 protein, rat; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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30. Kim J, Yamamoto F, Gondo S, Yanase T, Mukai T, Maeda M: 6-Deoxy-6-[131I]iodo-L-ascorbic acid for the in vivo study of ascorbate: autoradiography, biodistribution in normal and hypolipidemic rats, and in tumor-bearing nude mice. Biol Pharm Bull; 2009 Nov;32(11):1906-11
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  • [Title] 6-Deoxy-6-[131I]iodo-L-ascorbic acid for the in vivo study of ascorbate: autoradiography, biodistribution in normal and hypolipidemic rats, and in tumor-bearing nude mice.
  • Normal female rat distribution studies showed high and specific uptake of 6-deoxy-6-[(131)I]iodo-L-ascorbic acid (6-(131)IAsA) into the adrenal glands, known to highly express the ascorbate sodium-dependent vitamin C transporter-2 (SVCT-2), and the adrenal gland was clearly visualized by whole-body autoradiography.
  • Preinjection of sulfinpyrazone, a known blocker of ascorbate transport, with 6-(131)IAsA resulted in decreased uptake of radioactivity in rat adrenal glands compared to the control group, seemingly illustrating the participation of the SVCT transporter (probably the SVCT-2 subtype) in the uptake process in vivo.
  • 4-Aminopyrazolo[3,4-d]pyrimidine-induced hypolipidemic rats showed a 1.7-fold increase in adrenal uptake of radioactivity at 30 min postinjection of 6-(131)IAsA, compared to the control, with increased adrenal-to-liver and adrenal-to-kidney ratios.
  • To further characterize 6-(131)IAsA for its tumor uptake properties, biodistribution studies were also performed using male nude mice implanted with either Y-1 adrenocortical tumor cells or adrenal medulla-derived PC12 cells.
  • None of these tumors exhibited relevant uptake of 6-(131)IAsA while normal adrenal glands showed high uptake of radioactivity, suggesting that these tumors in this model have only a poor transport capacity for this agent.
  • The present study demonstrates that the use of radioiodinated 6-IAsA may help to obtain information about functional alterations in diseased adrenal glands, but it does not exhibit desirable properties as a tumor-seeking agent for ascorbic acid bioactivity.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Iodine Radioisotopes / pharmacokinetics. Lipids / blood. Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Ascorbic Acid / pharmacokinetics. Autoradiography. Chromatography, High Pressure Liquid. Female. Male. Mice. Mice, Nude. Rats. Rats, Sprague-Dawley. Tissue Distribution

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  • (PMID = 19881306.001).
  • [ISSN] 1347-5215
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / 6-deoxy-6-iodoascorbic acid; 0 / Iodine Radioisotopes; 0 / Lipids; PQ6CK8PD0R / Ascorbic Acid
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31. Zwermann O, Schulte DM, Reincke M, Beuschlein F: ACTH 1-24 inhibits proliferation of adrenocortical tumors in vivo. Eur J Endocrinol; 2005 Sep;153(3):435-44
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  • [Title] ACTH 1-24 inhibits proliferation of adrenocortical tumors in vivo.
  • OBJECTIVES: Although several lines of evidence suggest that the overall effects of the ACTH receptor, melanocortin 2 receptor (MC2-R), mediated signal transduction on adrenocortical growth and tumorigenesis are anti-proliferative, activation of MC2-R induces mitogens like jun, fos, and myc and activates the MAPK pathway.
  • In vivo, potential effects of endogenous ACTH on adrenal tumori-genesis can not be separated from effects of other POMC derived peptides.
  • METHODS: Murine adrenocortical tumor cells that lack MC2-R expression (Y6(pcDNA)) and Y6 cells stablely transfected with MC2-R (Y6(MC2-R)) were generated.
  • As a syngenic tumor model, LaHeF1/J mice simultaneously received 10(7) Y6(MC2-R) and Y6(pcDNA) subcutaneously, giving rise to MC2-R positive and negative tumors within the same animal.
  • Animals were treated for 3 weeks in groups of 12 according to the following schedule: group A, control animals receiving saline injection; group B, animals receiving 5.7 ng/injection of a slow release formula of ACTH 1-24 administered i.p. three times a week (aiming at a low physiologic dose); and group C, animals receiving 57 ng/injection of ACTH 1-24 (high physiological dose).
  • RESULTS: Twenty days of ACTH 1-24 treatment did not significantly affect corticosterone levels, endogenous ACTH levels or adrenal and thymus weight compared with saline injection.
  • However, ACTH 1-24 treatment of group B and C mice significantly reduced tumor weight in MC2-R positive tumors in a dose dependent manner (P = 0.03), while no significant difference in tumor mass was observed in MC2-R negative tumors.
  • PCNA and TUNEL staining, together with morphological characterization, demonstrated that these in vivo effects were due to reduced proliferation, while apoptosis and cellular hypertrophy within the tumor remained unchanged.
  • CONCLUSION: MC2-R expression is associated with a less aggressive adrenal tumor phenotype and anti-proliferative effects can be amplified through stimulation with physiological doses of ACTH.


32. Al-Hakim A, Rui X, Tsao J, Albert PR, Schimmer BP: Forskolin-resistant Y1 adrenal cell mutants are deficient in adenylyl cyclase type 4. Mol Cell Endocrinol; 2004 Feb 12;214(1-2):155-65
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  • [Title] Forskolin-resistant Y1 adrenal cell mutants are deficient in adenylyl cyclase type 4.
  • Four mutant clones independently derived from the Y1 mouse adrenocortical tumor cell line have adenylyl cyclase (AC) activities that are resistant to forskolin, a direct activator of AC.
  • Taken together, these observations indicate that AC-4 deficiency is a hallmark of the forskolin-resistant phenotype of these mutants and suggest that AC-4 is an important target of forskolin action in the Y1 adrenal cell line.
  • [MeSH-major] Adenylyl Cyclases / deficiency. Adrenal Cortex Neoplasms / pathology. Colforsin / pharmacology. Drug Resistance
  • [MeSH-minor] Animals. Cell Division. Cell Line, Tumor. Cell Size. Cyclic AMP / biosynthesis. Dose-Response Relationship, Drug. Mice. Mutation. Protein Isoforms / analysis. RNA, Messenger / analysis

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  • (PMID = 15062554.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 1F7A44V6OU / Colforsin; E0399OZS9N / Cyclic AMP; EC 4.6.1.1 / Adenylyl Cyclases; EC 4.6.1.1 / adenylyl cyclase 4
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33. Saeger W, Fassnacht M: [Effects of drugs on the adrenal cortex and its tumors]. Pathologe; 2006 Feb;27(1):61-4
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  • [Title] [Effects of drugs on the adrenal cortex and its tumors].
  • [Transliterated title] Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren.
  • The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids).
  • In animal experiments, the adrenostatic drug mitotane causes shrinkage of the cells of the fascicular and reticular zones, whereas metyrapone induces a decrease in the steroid producing organelle system and aminoglutethimide leads to an increase in lipids.
  • In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents / therapeutic use
  • [MeSH-minor] Adrenocorticotropic Hormone / physiology. Aminoglutethimide / adverse effects. Aminoglutethimide / therapeutic use. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Organelles / drug effects. Organelles / pathology

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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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34. Okayama S, Imagawa K, Naya N, Iwama H, Somekawa S, Kawata H, Horii M, Nakajima T, Uemura S, Saito Y: Blocking T-type Ca2+ channels with efonidipine decreased plasma aldosterone concentration in healthy volunteers. Hypertens Res; 2006 Jul;29(7):493-7
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  • [Title] Blocking T-type Ca2+ channels with efonidipine decreased plasma aldosterone concentration in healthy volunteers.
  • Efonidipine can block both L- and T- type Ca2+ channels.
  • In a previous in vitro study, we clarified that efonidipine dramatically suppresses aldosterone secretion from human adrenocortical tumor cells during angiotensin II (Ang II)- and K+-stimulation, whereas nifedipine, a dominant L-type Ca2+ channel antagonist, does not.
  • Hemodynamic parameters (pulse rate [PR] and blood pressure [BP]), plasma concentrations of neurohormonal factors (plasma renin activity, Ang II, aldosterone, and adrenocorticotropic hormone [ACTH]), and serum concentrations of Na+ and K+ were measured before and 6 h after administration of the agents.
  • All three agents had little effect on PR and BP.
  • Efonidipine decreased plasma aldosterone concentration despite the increase in plasma renin activity and Ang II, suggesting that T-type Ca2+ channels may also play an essential role in the secretion of aldosterone in healthy human volunteers.
  • [MeSH-major] Aldosterone / blood. Calcium Channel Blockers / pharmacology. Calcium Channels, T-Type / drug effects. Dihydropyridines / pharmacology. Nitrophenols / pharmacology
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Adult. Angiotensin II / blood. Cross-Over Studies. Depression, Chemical. Hemodynamics / physiology. Humans. Male. Neurotransmitter Agents / blood. Nifedipine / analogs & derivatives. Nifedipine / pharmacology. Organophosphorus Compounds / pharmacology. Renin / blood. Water-Electrolyte Balance / drug effects

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  • (PMID = 17044661.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Calcium Channels, T-Type; 0 / Dihydropyridines; 0 / Neurotransmitter Agents; 0 / Nitrophenols; 0 / Organophosphorus Compounds; 0214FUT37J / nilvadipine; 11128-99-7 / Angiotensin II; 40ZTP2T37Q / efonidipine; 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.23.15 / Renin; I9ZF7L6G2L / Nifedipine
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35. Müller-Vieira U, Angotti M, Hartmann RW: The adrenocortical tumor cell line NCI-H295R as an in vitro screening system for the evaluation of CYP11B2 (aldosterone synthase) and CYP11B1 (steroid-11beta-hydroxylase) inhibitors. J Steroid Biochem Mol Biol; 2005 Aug;96(3-4):259-70
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  • [Title] The adrenocortical tumor cell line NCI-H295R as an in vitro screening system for the evaluation of CYP11B2 (aldosterone synthase) and CYP11B1 (steroid-11beta-hydroxylase) inhibitors.
  • As a new pharmacological strategy for the treatment of these diseases, we propose the inhibition of the key enzyme of mineralcorticoid formation, CYP11B2 (aldosterone synthase).
  • For studies of the effects of CYP11B2 inhibitors on the adrenal cortex, we selected the NCI-H295R cell line which expresses most of the key enzymes necessary for steroidogenesis.
  • [MeSH-major] Cell Line, Tumor. Cytochrome P-450 CYP11B2 / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Steroid 11-beta-Hydroxylase / antagonists & inhibitors
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / drug effects. Adrenal Cortex / enzymology. Aldosterone / metabolism. Aromatase Inhibitors / pharmacology. Drug Evaluation, Preclinical. Fadrozole / pharmacology. Humans. Steroids / analysis. Steroids / metabolism

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  • (PMID = 15985365.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0 / Enzyme Inhibitors; 0 / Steroids; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; H3988M64PU / Fadrozole
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36. Frigeri C, Tsao J, Czerwinski W, Schimmer BP: Impaired steroidogenic factor 1 (NR5A1) activity in mutant Y1 mouse adrenocortical tumor cells. Mol Endocrinol; 2000 Apr;14(4):535-44
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  • [Title] Impaired steroidogenic factor 1 (NR5A1) activity in mutant Y1 mouse adrenocortical tumor cells.
  • Mutants isolated from the Y1 mouse adrenocortical tumor cell line (clones 10r-9 and 10r-6) are resistant to ACTH because they fail to express the melanocortin-2 receptor (MC2R).
  • Consistent with the observed impairment in SF1 function, other SF1-dependent genes, including Cyp11b1 and steroidogenic acute regulatory protein (StAR), were poorly expressed and global steroidogenesis, as evidenced by the metabolism of 22(R)-hydroxycholesterol to steroid products, was impaired.
  • These mutants thus provide an experimental paradigm to identify factors that influence SF1 function and to evaluate the relative importance of SF1 in the expression of genes essential for adrenal steroidogenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Mutation. Transcription Factors / genetics. Transcription Factors / metabolism
  • [MeSH-minor] Adrenal Cortex Hormones / biosynthesis. Adrenal Cortex Hormones / genetics. Adrenocorticotropic Hormone / pharmacology. Animals. DNA / metabolism. Drug Resistance. Fushi Tarazu Transcription Factors. Gene Expression. Homeodomain Proteins. Luciferases / genetics. Mice. Phosphoproteins / genetics. Promoter Regions, Genetic. Receptors, Corticotropin / genetics. Receptors, Cytoplasmic and Nuclear. Receptors, Melanocortin. Recombinant Fusion Proteins. Steroid 11-beta-Hydroxylase / genetics. Steroidogenic Factor 1. Transcription, Genetic. Tumor Cells, Cultured

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  • (PMID = 10770490.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / DNA-Binding Proteins; 0 / Fushi Tarazu Transcription Factors; 0 / Homeodomain Proteins; 0 / Phosphoproteins; 0 / Receptors, Corticotropin; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Melanocortin; 0 / Recombinant Fusion Proteins; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 0 / steroidogenic acute regulatory protein; 0 / steroidogenic factor 1, mouse; 9002-60-2 / Adrenocorticotropic Hormone; 9007-49-2 / DNA; EC 1.13.12.- / Luciferases; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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37. Murao K, Imachi H, Cao W, Yu X, Li J, Yoshida K, Ahmed RA, Matsumoto K, Nishiuchi T, Wong NC, Ishida T: High-density lipoprotein is a potential growth factor for adrenocortical cells. Biochem Biophys Res Commun; 2006 May 26;344(1):226-32
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  • [Title] High-density lipoprotein is a potential growth factor for adrenocortical cells.
  • The entry of cholesterol contained within high-density lipoprotein (HDL) into adrenocortical cells is mediated by a human homologue of SR-BI, CD36, and LIMPII Analogous-1 (CLA-1) and thus augmenting their growth.
  • To address the role of CLA-1, we created a mutant mCLA that lacked the C-terminal tail.
  • Expression of mCLA inhibited the proliferation of an adrenocortical cell line and the incorporation of [(3)H]thymidine into the cells.
  • These findings raise the possibility that the inhibitors of the effects of HDL may be of therapeutic value for adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex / drug effects. Growth Substances / physiology. Lipoproteins, HDL / pharmacology. Scavenger Receptors, Class B / physiology. Transcription Factor AP-1 / antagonists & inhibitors
  • [MeSH-minor] Androstadienes / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation. Mice. Mutation. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Promoter Regions, Genetic. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. Transcriptional Activation / drug effects


38. Breslin DS, Farling PA, Mirakhur RK: The use of remifentanil in the anaesthetic management of patients undergoing adrenalectomy: a report of three cases. Anaesthesia; 2003 Apr;58(4):358-62
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  • We describe the use of remifentanil in the anaesthetic management of three cases of open adrenalectomy, two for removal of a phaeochromocytoma and one for removal of an adrenal cortical tumour.
  • Although the use of remifentanil was associated with no adverse events in the patient undergoing resection of the adrenal cortical tumour, its administration was associated with significant hypotension and bradycardia in the two phaeochromocytoma patients, who had both been given alpha- and beta-adrenergic receptor blocking drugs before surgery.
  • It did not prevent the increases in blood pressure or plasma catecholamine levels associated with tumour manipulation in these patients.
  • Remifentanil should therefore be used with caution in patients receiving alpha- and beta-adrenergic receptor blocking drugs.
  • The use of potent vasodilators may still be necessary during tumour manipulation even if remifentanil is being infused.
  • [MeSH-minor] Adrenal Cortex Neoplasms / surgery. Epinephrine / blood. Female. Hemodynamics. Humans. Male. Middle Aged. Norepinephrine / blood. Pheochromocytoma / surgery

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  • (PMID = 12648118.001).
  • [ISSN] 0003-2409
  • [Journal-full-title] Anaesthesia
  • [ISO-abbreviation] Anaesthesia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anesthetics, Intravenous; 0 / Piperidines; P10582JYYK / remifentanil; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
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39. Cho YY, Kang MJ, Ogawa S, Yamashita Y, Fujino T, Yamamoto TT: Regulation by adrenocorticotropic hormone and arachidonate of the expression of acyl-CoA synthetase 4, an arachidonate-preferring enzyme expressed in steroidogenic tissues. Biochem Biophys Res Commun; 2000 Aug 11;274(3):741-5
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  • ACTH also induced ACS4 protein but not its mRNA in Y1 adrenocortical tumor cells, whereas both ACS4 mRNA and protein were increased by dibutyryl cAMP (db-cAMP) and forskolin.
  • [MeSH-major] Adrenocorticotropic Hormone / pharmacology. Arachidonic Acid / pharmacology. Coenzyme A Ligases / biosynthesis. Repressor Proteins. Saccharomyces cerevisiae Proteins
  • [MeSH-minor] Adrenal Cortex Neoplasms / enzymology. Adrenal Cortex Neoplasms / genetics. Animals. Female. Gene Expression Regulation, Enzymologic / drug effects. Mice. Mice, Inbred C57BL. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10924347.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Saccharomyces cerevisiae Proteins; 27YG812J1I / Arachidonic Acid; 9002-60-2 / Adrenocorticotropic Hormone; EC 6.2.1.- / Coenzyme A Ligases; EC 6.2.1.3 / FAA2 protein, S cerevisiae; EC 6.2.1.3 / long-chain-fatty-acid-CoA ligase
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40. Woods AM, McIlmoil CJ, Rankin EN, Packer AA, Stevens JC, Macievic JA, Brown AB, Porter JP, Judd AM: Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release. Domest Anim Endocrinol; 2008 Aug;35(2):217-30
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  • [Title] Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release.
  • The release of adrenal steroids during acute stress is primarily regulated by adrenocorticotropic hormone (ACTH).
  • In contrast, during chronic inflammatory stress additional factors are involved in regulating adrenal function.
  • In addition, LIF and LIF receptors (LIFR) are expressed in the human adrenal cortex and the human adrenocortical tumor cell line H295R.
  • However, the expression of LIF and LIFR in non-human adrenal glands and the effects of LIF on the release of cortisol from adrenal cells of non-human species have not been determined.
  • Furthermore, the effects of LIF on adrenal androgen release from all species are unknown.
  • In this study, immunohistochemistry, Western blots, RT-PCR, and nucleotide sequencing was utilized to demonstrate that LIF and its receptor are expressed throughout the bovine adrenal cortex.
  • Although LIF did not modify basal cortisol release from dispersed cells isolated from the bovine adrenal zona fasciculate, this cytokine increased ACTH-stimulated release of cortisol from these cells in a manner dependent on the LIF concentration and exposure interval.
  • In contrast, LIF in a concentration-dependent and time-dependent manner decreased basal and ACTH-stimulated adrenal androgen release from dispersed cells isolated from the bovine adrenal zona reticularis.
  • Because LIF release increases during inflammatory stress and this cytokine stimulates adrenal cortisol release and inhibits adrenal androgen release, this cytokine may play an important role in regulating the release of adrenal steroids during inflammatory stress.
  • [MeSH-major] Adrenal Cortex / metabolism. Androgens / metabolism. Cattle / metabolism. Hydrocortisone / metabolism. Leukemia Inhibitory Factor / metabolism. Receptors, OSM-LIF / metabolism
  • [MeSH-minor] Adrenocorticotropic Hormone / physiology. Animals. Blotting, Western / veterinary. Dose-Response Relationship, Drug. Female. Immunohistochemistry / veterinary. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / veterinary. Time Factors

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  • (PMID = 18638665.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Receptors, OSM-LIF; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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41. Frigeri C, Tsao J, Cordova M, Schimmer BP: A polymorphic form of steroidogenic factor-1 is associated with adrenocorticotropin resistance in y1 mouse adrenocortical tumor cell mutants. Endocrinology; 2002 Oct;143(10):4031-7
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  • [Title] A polymorphic form of steroidogenic factor-1 is associated with adrenocorticotropin resistance in y1 mouse adrenocortical tumor cell mutants.
  • ACTH resistance in mutant derivatives of the Y1 mouse adrenocortical tumor cell line results from a defect that affects the activity of steroidogenic factor-1 (SF1), thereby preventing the expression of the melanocortin-2 receptor.
  • The SF1(S172) allele represents a polymorphism rather than a spontaneous mutation because the two SF1 alleles can be traced to the hybrid mouse strain (C57L/J x A/HeJ) from which the original adrenal tumor was derived.
  • Our results indicate that the SF1(S172) allele is a marker of ACTH resistance in this family of adrenocortical tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / physiopathology. Adrenocorticotropic Hormone / pharmacology. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Polymorphism, Genetic / physiology. Transcription Factors / genetics
  • [MeSH-minor] Alleles. Animals. Base Sequence / genetics. Cells, Cultured. Fushi Tarazu Transcription Factors. Gene Amplification. Homeodomain Proteins. Mice. Molecular Sequence Data. Mutation / genetics. Receptors, Cytoplasmic and Nuclear. Species Specificity. Steroidogenic Factor 1. Tissue Distribution. Transcription, Genetic

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  • (PMID = 12239114.001).
  • [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 / DNA-Binding Proteins; 0 / Fushi Tarazu Transcription Factors; 0 / Homeodomain Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 0 / steroidogenic factor 1, mouse; 9002-60-2 / Adrenocorticotropic Hormone
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42. Forti FL, Schwindt TT, Moraes MS, Eichler CB, Armelin HA: ACTH promotion of p27(Kip1) induction in mouse Y1 adrenocortical tumor cells is dependent on both PKA activation and Akt/PKB inactivation. Biochemistry; 2002 Aug 6;41(31):10133-40
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  • [Title] ACTH promotion of p27(Kip1) induction in mouse Y1 adrenocortical tumor cells is dependent on both PKA activation and Akt/PKB inactivation.
  • Here we report antimitogenic mechanisms activated by the adrenocorticotropic hormone (ACTH) in the mouse Y1 adrenocortical tumor cell line.
  • ACTH rapidly promotes dephosphorylation of Akt/PKB in Y1 adrenal cells, while constitutively high levels of c-Ki-Ras.GTP remain unchanged.
  • ACTH and cAMP elevating agents fail to cause Akt/PKB dephosphorylation in PKA-deficient clonal mutants of Y1 cells.
  • In addition, cholera toxin, forskolin, and 8BrcAMP all mimic ACTH, causing dephosphorylation of Akt/PKB in wild-type Y1 cells.
  • ACTH is unable to prevent Akt/PKB phosphorylation, promoted by FGF2 in clonal lines of RasN17-Y1 transfectants displaying negligible levels of c-Ki-Ras.GTP.
  • ACTH promotes strong p27(Kip1) protein induction in wild-type Y1 adrenocortical cells but not in PKA-deficient Y1-clonal mutants nor in RasN17-Y1 transfectants.
  • PI3K inhibitors induce p27(Kip1) protein in all cells studied, i.e., wild type and transfectants.
  • The inverse correlation between levels of phosphorylated Akt/PKB and of p27(Kip1) protein caused by ACTH suggests a novel antimitogenic pathway activated by ACTH and mediated by cAMP/PKA in the mouse Y1 adrenocortical tumor cell line.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocorticotropic Hormone / physiology. Cyclic AMP-Dependent Protein Kinases / metabolism. Cyclins / biosynthesis. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Animals. Cyclin-Dependent Kinase Inhibitor p21. Mice. Phosphorylation. Proto-Oncogene Proteins c-akt. Tumor Cells, Cultured

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  • (PMID = 12146978.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Proto-Oncogene Proteins; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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43. Groussin L, Massias JF, Bertagna X, Bertherat J: Loss of expression of the ubiquitous transcription factor cAMP response element-binding protein (CREB) and compensatory overexpression of the activator CREMtau in the human adrenocortical cancer cell line H295R. J Clin Endocrinol Metab; 2000 Jan;85(1):345-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of expression of the ubiquitous transcription factor cAMP response element-binding protein (CREB) and compensatory overexpression of the activator CREMtau in the human adrenocortical cancer cell line H295R.
  • The pituitary hormone ACTH, acting through the cAMP pathway, plays a key role in proliferation and differentiation of the adrenal cortex.
  • Characterization of CRE-binding proteins was performed in the H295R cell line, which is considered a model for human adrenocortical tumor studies.
  • Western blot and RT-PCR studies demonstrated that CREB is not expressed in the human adrenocortical cancer cell line H295R, whereas it is expressed in normal adrenal.
  • High amounts of CREM proteins were present in H295R, demonstrating an overexpression of this transcription factor in the absence of CREB.
  • Furthermore, expression of the activator isoform CREMtau was very high in H295R compared to normal adrenal cortex.
  • Finally, gel retardation assays showed that CREM and ATF-1 are the nuclear proteins that specifically bind the CRE in H295R cells, whereas CREM binding to CRE is not observed in a CREB-expressing cell line.
  • This loss of CREB expression and the overexpression of CREM could be linked to cellular transformation, as the normal adrenal cortex express high levels of CREB and no or low levels of CREMtau.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Cyclic AMP Response Element-Binding Protein / biosynthesis. DNA-Binding Proteins / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Repressor Proteins / biosynthesis
  • [MeSH-minor] Activating Transcription Factor 1. Activating Transcription Factor 2. Blotting, Western. Cell Line. Cloning, Molecular. Cyclic AMP Response Element Modulator. Electrophoresis. Humans. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / biosynthesis. Transcription Factors / genetics. Up-Regulation / drug effects. Up-Regulation / genetics

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  • (PMID = 10634409.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Activating Transcription Factor 1; 0 / Activating Transcription Factor 2; 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA-Binding Proteins; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / Transcription Factors; 135844-64-3 / Cyclic AMP Response Element Modulator
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44. Louiset E, Isvi K, Gasc JM, Duparc C, Cauliez B, Laquerrière A, Kuhn JM, Lefebvre H: Ectopic expression of serotonin7 receptors in an adrenocortical carcinoma co-secreting renin and cortisol. Endocr Relat Cancer; 2008 Dec;15(4):1025-34
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  • [Title] Ectopic expression of serotonin7 receptors in an adrenocortical carcinoma co-secreting renin and cortisol.
  • Abnormal expression of membrane receptors has been previously described in benign adrenocortical neoplasms causing Cushing's syndrome.
  • In particular, we have observed that, in some adreno corticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia tissues, cortisol secretion is controlled by ectopic serotonin(7) (5-HT(7)) receptors.
  • The objective of the present study was to investigate in vitro the effect of serotonin (5-hydroxy tryptamine; 5-HT) on cortisol and renin production by a left adrenocortical carcinoma removed from a 48-year-old female patient with severe Cushing's syndrome and elevated plasma renin levels.
  • Tumor explants were obtained at surgery and processed for immunohistochemistry, in situ hybridization and cell culture studies.
  • In addition, immunohistochemistry showed the occurrence of 5-HT(7) receptor-like immunoreactivity in carcinoma cells. mRNAs encoding renin as well as renin-like immunoreactivity were detected in endothelial and tumor cells.
  • Cell incubation studies revealed that the adrenocortical tissue also released renin.
  • 5-HT(7) receptors, in an adrenocortical carcinoma.
  • Our results also indicate that 5-HT can influence the secretory activity of malignant adrenocortical tumors in an autocrine/paracrine manner.
  • The effects of 5-HT on adrenocortical tumor cells included a paradoxical inhibitory action on renin production and a stimulatory action on cortisol secretion involving 5-HT(7) receptors.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Hydrocortisone / metabolism. Receptors, Serotonin / metabolism. Renin / metabolism
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Angiotensin II / pharmacology. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. Female. Hormones / pharmacology. Humans. Immunoenzyme Techniques. In Situ Hybridization. Mast Cells / drug effects. Mast Cells / metabolism. Middle Aged. Phenols / pharmacology. Serotonin / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured / drug effects. Vasoconstrictor Agents / pharmacology

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  • (PMID = 18708508.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones; 0 / Phenols; 0 / Receptors, Serotonin; 0 / SB 269970; 0 / Sulfonamides; 0 / Vasoconstrictor Agents; 0 / serotonin 7 receptor; 11128-99-7 / Angiotensin II; 333DO1RDJY / Serotonin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.23.15 / Renin; WI4X0X7BPJ / Hydrocortisone
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45. Delhanty PJ, van Koetsveld PM, Gauna C, van de Zande B, Vitale G, Hofland LJ, van der Lely AJ: Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway. Am J Physiol Endocrinol Metab; 2007 Jul;293(1):E302-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway.
  • Ghrelin is expressed in normal human adrenocortical cells and induces their proliferation through growth hormone secretagogue receptor 1a (GHS-R1a).
  • Consequently, it was of interest to us to determine whether acylated ghrelin and its predominant serum isoform, unacylated ghrelin, also act as factors for adrenocortical carcinoma cell growth.
  • To examine a potential ghrelin-regulated system in adrenocortical tumors, we measured proliferative effects of acylated and unacylated ghrelin in the adrenocortical carcinoma cell lines SW-13 and NCI-H295R.
  • Acylated and unacylated ghrelin in the nanomolar range dose-dependently induced adrenocortical cell growth up to 200% of untreated controls, as measured by thymidine uptake and WST1 assay.
  • Acylated and unacylated ghrelin are potential auto/paracrine factors acting through an antiapoptotic pathway to stimulate adrenocortical tumor cell growth.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Apoptosis / drug effects. Cell Proliferation / drug effects. Peptide Hormones / pharmacology
  • [MeSH-minor] Acetylation. Cell Cycle / drug effects. Ghrelin. Humans. Protein Isoforms / pharmacology. Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Corticotropin-Releasing Hormone / metabolism. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Receptors, Ghrelin. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 17405826.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRF receptor type 2; 0 / Ghrelin; 0 / Peptide Hormones; 0 / Protein Isoforms; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin
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