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Increased AR expression in castration-resistant prostate cancer rapidly induces AR signaling reprogramming with the collaboration of EZH2

Title: Increased AR expression in castration-resistant prostate cancer rapidly induces AR signaling reprogramming with the collaboration of EZH2
Authors: Maryam Labaf; Muqing Li; Lily Ting; Breelyn Karno; Songqi Zhang; Shuai Gao; Susan Patalano; Jill A. Macoska; Kourosh Zarringhalam; Dong Han; Changmeng Cai
Source: Frontiers in Oncology, Vol 12 (2022)
Publisher Information: Frontiers Media S.A.
Publication Year: 2022
Collection: Directory of Open Access Journals: DOAJ Articles
Subject Terms: androgen; androgen receptor; AR; prostate cancer; androgen-deprivation therapy; CRPC; Neoplasms. Tumors. Oncology. Including cancer and carcinogens; RC254-282
Description: 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 repair pathways. Moreover, using a recently developed bioinformatic tool, we predicted the involvement of EZH2 in this AR reprogramming and subsequently identified a subset of AR/EZH2 co-targeting genes, which are overexpressed in CRPC and associated with worse patient outcomes. Mechanistically, we found that AR-EZH2 interaction is impaired by the pre-castration level of androgens but can be recovered by the post-castration level of androgens. Overall, our study provides new molecular insights into AR signaling reprogramming with the engagement of specific epigenetic factors.
Document Type: article in journal/newspaper
Language: English
Relation: https://www.frontiersin.org/articles/10.3389/fonc.2022.1021845/full; https://doaj.org/toc/2234-943X; https://doaj.org/article/5e90a30cdd9c442d9a77e09c7e16a41f
DOI: 10.3389/fonc.2022.1021845
Availability: https://doi.org/10.3389/fonc.2022.1021845; https://doaj.org/article/5e90a30cdd9c442d9a77e09c7e16a41f
Accession Number: edsbas.90FE042C
Database: BASE