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

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

PROVIDER: PRJNA685099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13249800.fastq.gz	Fastqsanger.gz
	SRR13259800.fastq.gz	Fastqsanger.gz
	SRR13249801.fastq.gz	Fastqsanger.gz
	SRR13259801.fastq.gz	Fastqsanger.gz
	SRR13249802.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 [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 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

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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: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 | GSE163145 | GEO

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

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Androgen receptor condensates as drug targets

Project description:Androgen receptor condensates as drug targets

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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. 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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Androgen receptor condensates as drug targets

Project description:Transcription factors are among the most attractive therapeutic targets but are considered largely undruggable. Here we provide evidence that small molecule-mediated partitioning of the androgen receptor, an oncogenic transcription factor, into phase-separated condensates has therapeutic effect in prostate cancer. We show that the phase separation capacity of the androgen receptor is driven by aromatic residues and short unstable helices in its intrinsically disordered activation domain. Based on this knowledge, we developed tool compounds that covalently attach aromatic moieties to cysteines in the receptors’ activation domain. The compounds enhanced partitioning of the receptor into condensates, facilitated degradation of the receptor, inhibited androgen receptor-dependent transcriptional programs, and had antitumorigenic effect in mouse models of prostate cancer and castration resistant prostate cancer. These results establish a generalizable framework to target the phase-separation capacity of intrinsically disordered regions in oncogenic transcription factors and other disease-associated proteins with therapeutic intent.

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Androgen receptor RIME using LNCaP cells

Project description:Rapid immunoprecipitation mass spectrometry of endogenous protein (RIME) was conducted to examine interactome of androgen receptor (AR) in LNCaP cells.

2021-09-10 | PXD024030 | JPOST Repository

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