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MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets

ABSTRACT: MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets

PROVIDER: PRJNA685750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13259800.fastq.gz	Fastqsanger.gz
	SRR13259801.fastq.gz	Fastqsanger.gz
	SRR13259802.fastq.gz	Fastqsanger.gz
	SRR13259803.fastq.gz	Fastqsanger.gz
	SRR13259804.fastq.gz	Fastqsanger.gz

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MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets

Project description:MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets

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MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [ChIP-Seq]

Project description:MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [ChIP-Seq]

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MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [RNA-Seq]

Project description:MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [RNA-Seq]

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MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets

Project description:c-MYC (MYC) is a major driver of prostate cancer tumorigenesis and progression. Although MYC is overexpressed in both early and metastatic disease and associated with poor survival, its impact on prostate transcriptional reprogramming remains elusive. We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression. Importantly, analyses of clinical specimens revealed that concurrent low AR and high MYC transcriptional programs accelerate prostate cancer progression toward a metastatic, castration-resistant disease. Data integration of single-cell transcriptomics together with chromatin immunoprecipitation followed by sequencing (ChIP-seq) revealed an increased RNA polymerase II (Pol II) promoter-proximal pausing at AR-dependent genes following MYC overexpression without an accompanying deactivation of AR-bound enhancers. Altogether, our findings suggest that MYC overexpression antagonizes the canonical AR transcriptional program and contributes to prostate tumor initiation and progression by disrupting transcriptional pause release at AR-regulated genes.

2022-03-28 | GSE163316 | GEO

MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [RNA-Seq]

2022-03-28 | GSE163143 | GEO

MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets at androgen receptor targets [ChIP-Seq]

2022-03-28 | GSE163145 | GEO

MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets.

Project description:c-MYC (MYC) is a major driver of prostate cancer tumorigenesis and progression. Although MYC is overexpressed in both early and metastatic disease and associated with poor survival, its impact on prostate transcriptional reprogramming remains elusive. We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression. Analyses of clinical specimens reveal that concurrent low AR and high MYC transcriptional programs accelerate prostate cancer progression toward a metastatic, castration-resistant disease. Data integration of single-cell transcriptomics together with ChIP-seq uncover an increase in RNA polymerase II (Pol II) promoter-proximal pausing at AR-dependent genes following MYC overexpression without an accompanying deactivation of AR-bound enhancers. Altogether, our findings suggest that MYC overexpression antagonizes the canonical AR transcriptional program and contributes to prostate tumor initiation and progression by disrupting transcriptional pause release at AR-regulated genes.

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Brd4 and JMJD6-associated Anti-pause Enhancers in Regulation of Transcriptional Pause Release

Project description:Distal enhancers characterized by H3K4me1 mark play critical roles in developmental and transcriptional programs. However, potential roles of specific distal regulatory elements in regulating RNA Polymerase II (Pol II) promoter-proximal pause release remain poorly investigated. Here we report that a unique cohort of jumonji C domain-containing protein 6 (JMJD6) and bromodomain-containing protein 4 (Brd4) co-bound distal enhancers, termed anti-pause enhancers (A-PEs), regulate promoter-proximal pause release of a large subset of transcription units via long-range interactions. Brd4-dependent JMJD6 recruitment on A-PEs mediates erasure of H4R3me2(s), which is directly read by 7SK snRNA, and decapping/demethylation of 7SK snRNA, ensuring the dismissal of the 7SKsnRNA/HEXIM inhibitory complex. The interactions of both JMJD6 and Brd4 with the P-TEFb complex permit its activation and pause release of regulated coding genes. The functions of JMJD6/ Brd4-associated dual histone and RNA demethylase activity on anti-pause enhancers have intriguing implications for these proteins in development, homeostasis and disease. All Gro-seq(s) were designed to reveal the transcriptional targets of JMJD6 and Brd4, and assess the role of JMJD6 and Brd4 in Pol II promoter-proximal pause release. All ChIP-seq(s) were designed to understand the unique features, associated molecular mechanisms and functions of the anti-pause enhancers (A-PEs) discovered in the current study.

2014-01-14 | E-GEOD-51633 | biostudies-arrayexpress

Myo6 regulate transcriptional pause release

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Brd4 and JMJD6-associated Anti-pause Enhancers in Regulation of Transcriptional Pause Release

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