Increased <i>AR</i> expression in castration-resistant prostate cancer rapidly induces AR signaling reprogramming with the collaboration of EZH2.

ABSTRACT: Elevated androgen receptor (AR) expression is a hallmark of castration-resistant prostate cancer (CRPC) and contributes to the restoration of AR signaling under the conditions of androgen deprivation. However, whether overexpressed AR alone with the stimulation of castrate levels of androgens can be sufficient to induce the reprogramming of AR signaling for the adaptation of prostate cancer (PCa) cells remains unclear. In this study, we used a PCa model with inducible overexpression of AR to examine the acute effects of AR overexpression on its cistrome and transcriptome. Our results show that overexpression of AR alone in conjunction with lower androgen levels can rapidly redistribute AR chromatin binding and activates a distinct transcription program that is enriched for DNA damage repai

SUBMITTER: Labaf M 

PROVIDER: S-EPMC9669968 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature