scholarly journals The prognostic role of steroid hormone receptor signaling pathways in urothelial carcinoma

2020 ◽  
Vol 9 (10) ◽  
pp. 6596-6608
Author(s):  
Yujiro Nagata ◽  
Hiroshi Miyamoto
PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46985 ◽  
Author(s):  
Lisa M. Privette Vinnedge ◽  
Shuk-Mei Ho ◽  
Kathryn A. Wikenheiser-Brokamp ◽  
Susanne I. Wells

2003 ◽  
Vol 17 (10) ◽  
pp. 2039-2052 ◽  
Author(s):  
Kathleen H. Burns ◽  
Julio E. Agno ◽  
Lei Chen ◽  
Bisong Haupt ◽  
Samuel C. Ogbonna ◽  
...  

2005 ◽  
Vol 102 (8) ◽  
pp. 2707-2712 ◽  
Author(s):  
J. Zhang ◽  
J. Simisky ◽  
F. T. F. Tsai ◽  
D. S. Geller

1999 ◽  
Vol 13 (7) ◽  
pp. 1141-1154 ◽  
Author(s):  
Ana I. Castillo ◽  
Ana M. Jimenez-Lara ◽  
Rosa M. Tolon ◽  
Ana Aranda

Abstract PRL gene expression is dependent on the presence of the pituitary-specific transcription factor GHF-1/Pit-1, which is transcribed in a highly restricted manner in cells of the anterior pituitary. In pituitary GH3 cells, vitamin D increases the levels of PRL transcripts and stimulates the PRL promoter. We have analyzed the role of GHF-1 and of the vitamin D receptor (VDR) to confer vitamin D responsiveness to the PRL promoter. For this purpose we have used nonpituitary HeLa cells, which do not express GHF-1. We found that VDR activates the PRL promoter both in a ligand-dependent and -independent manner through a sequence located between positions− 45/−27 in the proximal 5′-flanking region. This sequence also confers VDR and vitamin D responsiveness to a heterologous promoter. In the context of the PRL gene, VDR requires the presence of GHF-1 to activate the promoter. Truncation of the last 12 C-terminal amino acids of VDR, which contain the ligand-dependent activation function (AF2), abolishes regulation by vitamin D, suggesting that binding of coactivators to this region mediates ligand-dependent stimulation of the PRL promoter by the receptor. Indeed, expression of the coactivators, steroid hormone receptor coactivator-1 (SRC-1) and CREB-binding protein (CBP), significantly enhances the stimulatory effect of vitamin D mediated by the wild-type VDR but not by the AF2 mutant receptor. Furthermore, CBP also increases the activation of the PRL promoter by GHF-1 and the ligand-independent activation by both wild-type and mutant VDR.


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