Increased nuclear factor I-mediated chromatin access drives transition to androgen receptor splice variant dependence in prostate cancer.

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Tác giả: Steven P Balk, Myles Brown, Laura Cato, Shaoyong Chen, Eva Corey, Betul Ersoy-Fazlioglu, Matthew L Freedman, Nathan A Lack, Irene I Lee, Jiaqian Liang, Henry W Long, Peter S Nelson, Mannan Nouri, Larysa Poluben, Xintao Qiu, Joshua W Russo, Ji-Heui Seo, Adam G Sowalsky, Andreas Varkaris, Olga Voznesensky

Ngôn ngữ: eng

Ký hiệu phân loại: 946.7 *Eastern Spain and Andorra

Thông tin xuất bản: United States : Cell reports , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 720458

Androgen receptor (AR) splice variants, of which ARv7 is the most common, are increased in castration-resistant prostate cancer, but the extent to which they drive AR activity is unclear. We generated a subline of VCaP cells (VCaP16) that is resistant to the AR inhibitor enzalutamide (ENZ). AR activity in VCaP16 is driven by ARv7, independently of full-length AR (ARfl), and its cistrome and transcriptome mirror those of ARfl in VCaP cells. ARv7 expression increases rapidly in response to ENZ, but there is a delay in gaining chromatin binding and transcriptional activity, which is associated with increased chromatin accessibility. AR and nuclear factor I (NFI) motifs are most enriched at more accessible sites, and NFIB/X knockdown greatly diminishes ARv7 function. These findings indicate that ARv7 can drive the AR program but that its activity is dependent on adaptations that increase chromatin accessibility to enhance its intrinsically weak chromatin binding.
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