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ARv7 Represses Tumor-Suppressor Genes in Castration-Resistant Prostate Cancer.


Cato L, de Tribolet-Hardy J, Lee I, Rottenberg JT, Coleman I, Melchers D, Houtman R, Xiao T, Li W, Uo T, Sun S, Kuznik NC, Göppert B, Ozgun F, van Royen ME, Houtsmuller AB, Vadhi R, Rao PK, Li L, Balk SP, Den RB, Trock BJ, Karnes RJ, Jenkins RB, Klein EA,

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.

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Antibody

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Published
March, 2019

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Products used in this publication

  • Antibody ChIP-seq grade icon
    C15410196
    H3K27ac Antibody - ChIP-seq Grade

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