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

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.

SUBMITTER: Cato L

PROVIDER: S-EPMC7246081 | biostudies-literature |

REPOSITORIES: biostudies-literature

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ARv7 represses tumor suppressors genes in castration-resistant prostate cancer

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A Novel, Circulating Tumor Cell Enrichment Method Reduces ARv7 False Positivity in Patients with Castration-Resistant Prostate Cancer.

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