| Literature DB >> 30773341 |
Laura Cato1, Jonas de Tribolet-Hardy2, Irene Lee1, Jaice T Rottenberg1, Ilsa Coleman3, Diana Melchers4, René Houtman4, Tengfei Xiao5, Wei Li6, Takuma Uo7, Shihua Sun7, Nane C Kuznik8, Bettina Göppert9, Fatma Ozgun10, Martin E van Royen11, Adriaan B Houtsmuller11, Raga Vadhi1, Prakash K Rao1, Lewyn Li1, Steven P Balk12, Robert B Den13, Bruce J Trock14, R Jeffrey Karnes14, Robert B Jenkins15, Eric A Klein16, Elai Davicioni17, Friederike J Gruhl9, Henry W Long1, X Shirley Liu6, Andrew C B Cato8, Nathan A Lack18, Peter S Nelson3, Stephen R Plymate19, Anna C Groner20, Myles Brown21.
Abstract
Androgen deprivation therapy for prostate cancer (PCa) benefits patients with early disease, but becomes ineffective as PCa progresses to a castration-resistant state (CRPC). Initially CRPC remains dependent on androgen receptor (AR) signaling, often through increased expression of full-length AR (ARfl) or expression of dominantly active splice variants such as ARv7. We show in ARv7-dependent CRPC models that ARv7 binds together with ARfl to repress transcription of a set of growth-suppressive genes. Expression of the ARv7-repressed targets and ARv7 protein expression are negatively correlated and predicts for outcome in PCa patients. Our results provide insights into the role of ARv7 in CRPC and define a set of potential biomarkers for tumors dependent on ARv7.Entities:
Keywords: AR variant v7 (ARv7); androgen receptor (AR); castration-resistant prostate cancer (CRPC); transcription
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Year: 2019 PMID： 30773341 PMCID： PMC7246081 DOI： 10.1016/j.ccell.2019.01.008
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743