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The transcriptional equilibration between androgen receptor and MYC signatures during prostate cancer transition centralizes on a distal developmental super-enhancer circuitry (4C-Seq)

ABSTRACT: We used RNA-Seq, ChIP-Seq and 4C-Seq to assess the role of MYC in the transcriptional repression induced by DHT in prostate cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157106 | GEO | 2021/10/29

REPOSITORIES: GEO

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The transcriptional equilibration between androgen receptor and MYC signatures during prostate cancer transition centralizes on a distal developmental super-enhancer circuitry (HiChIP)

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The transcriptional equilibration between androgen receptor and MYC signatures during prostate cancer transition centralizes on a distal developmental super-enhancer circuitry (ChIP-Seq)

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Androgen receptor and MYC equilibration centralizes on developmental super-enhancer.

Project description:Androgen receptor (AR) in prostate cancer (PCa) can drive transcriptional repression of multiple genes including MYC, and supraphysiological androgen is effective in some patients. Here, we show that this repression is independent of AR chromatin binding and driven by coactivator redistribution, and through chromatin conformation capture methods show disruption of the interaction between the MYC super-enhancer within the PCAT1 gene and the MYC promoter. Conversely, androgen deprivation in vitro and in vivo increases MYC expression. In parallel, global AR activity is suppressed by MYC overexpression, consistent with coactivator redistribution. These suppressive effects of AR and MYC are mitigated at shared AR/MYC binding sites, which also have markedly higher levels of H3K27 acetylation, indicating enrichment for functional enhancers. These findings demonstrate an intricate balance between AR and MYC, and indicate that increased MYC in response to androgen deprivation contributes to castration-resistant PCa, while decreased MYC may contribute to responses to supraphysiological androgen therapy.

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