scholarly journals SUN-002 Control of Metastasis by DAX-1 in Prostate Cancer Cells, an Androgen-Induced Orphan Nuclear Receptor

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Roxxana Beltran ◽  
Christina Tzagarakis-Foster
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Nuclear Receptor ◽  
Orphan Nuclear Receptor ◽  
Prostate Cancer Cells

scholarly journals Activation of the orphan nuclear receptor RORα counteracts the proliferative effect of fatty acids on prostate cancer cells: Crucial role of 5-lipoxygenase

2004 ◽  
Vol 112 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Roberta M. Moretti ◽  
Marina Montagnani Marelli ◽  
Angelo Sala ◽  
Marcella Motta ◽  
Patrizia Limonta
Keyword(s):  
Prostate Cancer ◽  
Fatty Acids ◽  
Cancer Cells ◽  
Nuclear Receptor ◽  
Crucial Role ◽  
Orphan Nuclear Receptor ◽  
Prostate Cancer Cells ◽  
Proliferative Effect

scholarly journals Activation of the orphan nuclear receptor ROR? induces growth arrest in androgen-independent DU 145 prostate cancer cells

The Prostate ◽  
2001 ◽  
Vol 46 (4) ◽  
pp. 327-335 ◽  
Author(s):  
Roberta M. Moretti ◽  
Marina Montagnani Marelli ◽  
Marcella Motta ◽  
Donatella Polizzi ◽  
Silvia Monestiroli ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Nuclear Receptor ◽  
Growth Arrest ◽  
Orphan Nuclear Receptor ◽  
Prostate Cancer Cells ◽  
Androgen Independent

scholarly journals Recruitment of β-Catenin by Wild-Type or Mutant Androgen Receptors Correlates with Ligand-Stimulated Growth of Prostate Cancer Cells

2004 ◽  
Vol 18 (10) ◽  
pp. 2388-2401 ◽  
Author(s):  
David Masiello ◽  
Shao-Yong Chen ◽  
Youyuan Xu ◽  
Manon C. Verhoeven ◽  
Eunis Choi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Nuclear Receptor ◽  
Specific Antigen ◽  
Prostate Cancer Cells ◽  
Prostate Cell ◽  
Nuclear Receptor Corepressor ◽  
Prostate Cancers

Abstract Prostate cancers respond to treatments that suppress androgen receptor (AR) function, with bicalutamide, flutamide, and cyproterone acetate (CPA) being AR antagonists in clinical use. As CPA has substantial agonist activity, it was examined to identify AR coactivator/corepressor interactions that may mediate androgen-stimulated prostate cancer growth. The CPA-liganded AR was coactivated by steroid receptor coactivator-1 (SRC-1) but did not mediate N-C terminal interactions or recruit β-catenin, indicating a nonagonist conformation. Nonetheless, CPA did not enhance AR interaction with nuclear receptor corepressor, whereas the AR antagonist RU486 (mifepristone) strongly stimulated AR-nuclear receptor corepressor binding. The role of coactivators was further assessed with a T877A AR mutation, found in LNCaP prostate cancer cells, which converts hydroxyflutamide (HF, the active flutamide metabolite) into an agonist that stimulates LNCaP cell growth. The HF and CPA-liganded T877A ARs were coactivated by SRC-1, but only the HF-liganded T877A AR was coactivated by β-catenin. L-39, a novel AR antagonist that transcriptionally activates the T877A AR, but still inhibits LNCaP growth, similarly mediated recruitment of SRC-1 and not β-catenin. In contrast, β-catenin coactivated a bicalutamide-responsive mutant AR (W741C) isolated from a bicalutamide-stimulated LNCaP subline, further implicating β-catenin recruitment in AR-stimulated growth. Androgen-stimulated prostate-specific antigen gene expression in LNCaP cells could be modulated by β-catenin, and endogenous c-myc expression was repressed by dihydrotestosterone, but not CPA. These results indicate that interactions between AR and β-catenin contribute to prostate cell growth in vivo, although specific growth promoting genes positively regulated by AR recruitment of β-catenin remain to be identified.

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