scholarly journals Transforming growth factor beta1 inhibits aldosterone and cortisol production in the human adrenocortical cell line NCI-H295R through inhibition of CYP11B1 and CYP11B2 expression

2003 ◽  
Vol 176 (1) ◽  
pp. 69-82 ◽  
Author(s):  
P Liakos ◽  
D Lenz ◽  
R Bernhardt ◽  
JJ Feige ◽  
G Defaye
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Tumor Cell ◽  
Cell Line ◽  
Transforming Growth Factor ◽  
Tumor Cell Line ◽  
Mrna Levels ◽  
Adrenocortical Tumor ◽  
Adrenocortical Cell ◽  
Transforming Growth Factor Beta1

Transforming growth factor beta1 (TGFbeta1) has been shown to exert strong inhibitory effects on adrenocortical cell steroidogenesis. However, the molecular targets of TGFbeta1 in adrenocortical cells appear to differ between species. Here, we report the first characterization of the regulatory effects of TGFbeta1 on the steroidogenic functions of the human adrenocortical tumor cell line NCI-H295R. After treatment with 2 ng/ml TGFbeta1 for 24 h, basal production of corticosterone, cortisol and androstenedione was dramatically decreased. When TGFbeta1 was added simultaneously with forskolin, the production of cortisol and 11-hydroxyandrostenedione was decreased by 85% whereas that of deoxycortisol was increased. When TGFbeta1 was added simultaneously with angiotensin II, aldosterone production was reduced by 80%. We observed that TGFbeta1 strongly inhibits forskolin-induced steroid 11beta-hydroxylase activity and CYP11B1 mRNA levels, as well as angiotensin II-induced aldosterone synthase activity and CYP11B2 mRNA levels. CYP11B1 and CYP11B2 gene products thus appear as the major steroidogenic enzymes down-regulated by TGFbeta1 in the human adrenocortical tumor cell line NCI-H295R.

scholarly journals CisModification of the Steroid 21-Hydroxylase Gene Prevents Its Expression in the Y1 Mouse Adrenocortical Tumor Cell Line

1990 ◽  
Vol 4 (8) ◽  
pp. 1144-1152 ◽  
Author(s):  
Moshe Szyf ◽  
David S. Milstone ◽  
Bernard P. Schimmer ◽  
Keith L. Parker ◽  
J. G. Seidman
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Tumor Cell Line ◽  
Adrenocortical Tumor ◽  
Hydroxylase Gene

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 ◽  
Vol 42 (7) ◽  
pp. 2116-2121 ◽  
Author(s):  
Telma T. Schwindt ◽  
Fábio L. Forti ◽  
Maria Ap. Juliano ◽  
Luiz Juliano ◽  
Hugo A. Armelin
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Cyclin D1 ◽  
Cell Line ◽  
Arginine Vasopressin ◽  
Tumor Cell Line ◽  
Adrenocortical Tumor

scholarly journals A colony-stimulating factor 1 (CSF-1) receptor/platelet-derived growth factor-beta receptor gene fusion confers CSF-1 independence and tumorigenicity on a c-myc-immortalized monocyte cell line.

1992 ◽  
Vol 12 (1) ◽  
pp. 386-393
Author(s):  
M R Eccles ◽  
F J King ◽  
M D Cole
Keyword(s):  
Growth Factor ◽  
Tumor Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Tumor Cell Line ◽  
Platelet Derived Growth Factor ◽  
Colony Stimulating Factor ◽  
Amino Terminal ◽  
Monocyte Cell ◽  
Stimulating Factor

Monocytes and macrophages express the receptor for the hematopoietic growth factor colony-stimulating factor 1 (CSF-1) and require this factor for growth in culture. A murine monocyte tumor cell line that lacks the usual requirement for CSF-1 was isolated. On the basis of the similarity of the structures of the CSF-1 and platelet-derived growth factor (PDGF) receptors and because monocytes normally secrete PDGF, we analyzed the tumor cell line for anomalous expression of the PDGF-R beta gene. Two different cDNAs that each contain sequences corresponding to the complete coding sequence of PDGF-R beta fused (in frame) to the amino-terminal half of the CSF-1 receptor were isolated. Introduction of these PDGF-R beta-related cDNAs into two partially transformed, CSF-1-dependent monocyte cell lines resulted in autonomous growth and cell transformation. These monocyte cell lines exhibit a novel form of growth factor receptor activation that can lead to oncogenic growth in collaboration with the c-myc oncogene.

A colony-stimulating factor 1 (CSF-1) receptor/platelet-derived growth factor-beta receptor gene fusion confers CSF-1 independence and tumorigenicity on a c-myc-immortalized monocyte cell line

1992 ◽  
Vol 12 (1) ◽  
pp. 386-393
Author(s):  
M R Eccles ◽  
F J King ◽  
M D Cole
Keyword(s):  
Growth Factor ◽  
Tumor Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Tumor Cell Line ◽  
Platelet Derived Growth Factor ◽  
Colony Stimulating Factor ◽  
Amino Terminal ◽  
Monocyte Cell ◽  
Stimulating Factor

Monocytes and macrophages express the receptor for the hematopoietic growth factor colony-stimulating factor 1 (CSF-1) and require this factor for growth in culture. A murine monocyte tumor cell line that lacks the usual requirement for CSF-1 was isolated. On the basis of the similarity of the structures of the CSF-1 and platelet-derived growth factor (PDGF) receptors and because monocytes normally secrete PDGF, we analyzed the tumor cell line for anomalous expression of the PDGF-R beta gene. Two different cDNAs that each contain sequences corresponding to the complete coding sequence of PDGF-R beta fused (in frame) to the amino-terminal half of the CSF-1 receptor were isolated. Introduction of these PDGF-R beta-related cDNAs into two partially transformed, CSF-1-dependent monocyte cell lines resulted in autonomous growth and cell transformation. These monocyte cell lines exhibit a novel form of growth factor receptor activation that can lead to oncogenic growth in collaboration with the c-myc oncogene.

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