The zinc finger protein Ras-responsive element binding protein-1 is a coregulator of the androgen receptor: Implications for the role of the Ras pathway in enhancing androgenic signaling in prostate cancer

Author(s):  
Yingming Li ◽  
Kenneth S. Koeneman
2011 ◽  
Vol 130 (4) ◽  
pp. 885-895 ◽  
Author(s):  
Mette Opstrup Abildgaard ◽  
Michael Borre ◽  
Martin Mørck Mortensen ◽  
Benedicte P. Ulhøi ◽  
Niels Tørring ◽  
...  

2013 ◽  
Vol 185 (2) ◽  
pp. 717-725 ◽  
Author(s):  
Bo Liu ◽  
Dianming Jiang ◽  
Yunsheng Ou ◽  
Zhenming Hu ◽  
Jianxin Jiang ◽  
...  

2005 ◽  
Vol 34 (1) ◽  
pp. 107-118 ◽  
Author(s):  
J Kim ◽  
L Jia ◽  
M R Stallcup ◽  
G A Coetzee

Androgen-independent prostate cancer is a lethal form of the disease that is marked by metastasis and rapid proliferation in its final stages. As no effective therapy for this aggressive tumor currently exists, it is imperative to elucidate and target the mechanisms involved in the progression to androgen independence. Accumulating evidence indicates that aberrant activation of androgen receptor (AR) via signal transduction pathways, AR gene mutation and/or amplification, and/or coregulator alterations may contribute to the progression of prostate cancer. In the present study, the effects of protein kinase A (PKA) signaling and its downstream factors on AR activity at the prostate-specific antigen (PSA) gene were tested. Activation of PKA by forskolin resulted in enhanced androgen-induced expression of the PSA gene, an effect that was blocked by the AR antagonist, bicalutamide. Interestingly, when either p300 or CBP was overexpressed, PKA activation was sufficient to stimulate PSA promoter-driven transcription in the absence of androgen, which was not inhibited by bicalutamide. PKA activation did not significantly alter AR protein levels but significantly increased the phosphorylated form of its downstream effector, cAMP responsive element-binding protein (CREB) in the presence of androgen. Furthermore, chromatin immunoprecipitation showed that the combination of androgen and forskolin increased phosphorylated CREB occupancy, which was accompanied by histone acetylation, at the putative cAMP responsive element located in the 5′ upstream regulatory region of the PSA gene. Remarkably, mammalian two-hybrid assay indicated that p300/CBP may bridge the interaction between AR and CREB, suggesting a novel enhanceosomal cooperation. These results demonstrate an intriguing interplay between a signal transduction pathway, coactivator overexpression and AR signaling as a possible combined mechanism of progression to androgen-independent prostate cancer.


2010 ◽  
Vol 91 (6) ◽  
pp. 1494-1502 ◽  
Author(s):  
S. Kaufmann ◽  
M. Sauter ◽  
M. Schmitt ◽  
B. Baumert ◽  
B. Best ◽  
...  

The Prostate ◽  
2011 ◽  
Vol 71 (14) ◽  
pp. 1518-1524 ◽  
Author(s):  
Jing Zou ◽  
Beatrice C. Milon ◽  
Mohamed M. Desouki ◽  
Leslie C. Costello ◽  
Renty B. Franklin

2013 ◽  
Author(s):  
Raffaella Spina ◽  
Gessica Filocamo ◽  
Enrico Iaccino ◽  
Stefania Scicchitano ◽  
Michela Lupia ◽  
...  

2018 ◽  
Vol 28 (3) ◽  
pp. 217-221 ◽  
Author(s):  
Gaurav Gupta ◽  
Mary Bebawy ◽  
Terezinha de Jesus Andreoli Pinto ◽  
Dinesh Kumar Chellappan ◽  
Anurag Mishra ◽  
...  

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