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SPOP mutation reshapes chromatin landscape and transcriptional response to androgens [RNA-seq]

ABSTRACT: SPOP mutation reshapes chromatin landscape and transcriptional response to androgens [RNA-seq]

PROVIDER: PRJNA630382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11687400.fastq.gz	Fastqsanger.gz
	SRR11687401.fastq.gz	Fastqsanger.gz
	SRR11687402.fastq.gz	Fastqsanger.gz
	SRR11687403.fastq.gz	Fastqsanger.gz
	SRR11687404.fastq.gz	Fastqsanger.gz

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SPOP mutation reshapes chromatin landscape and transcriptional response to androgens.

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SPOP mutation reshapes chromatin landscape and transcriptional response to androgens [RNA-seq]

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SPOP mutation reshapes chromatin landscape and transcriptional response to androgens.

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effects of SPOP mutation in DU145 cells

Project description:We aimed at analyzing the transcriptome changes associated with SPOP mutation in DU145 cells

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SPOP mutation - SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling

Project description:Recurrent point mutations in SPOP define a distinct molecular subclass of prostate cancer. Here, we describe the first mouse model showing that mutant SPOP drives prostate tumorigenesis in vivo. Conditional expression of mutant SPOP in the prostate dramatically altered phenotypes in the setting of Pten loss, with early neoplastic lesions (high-grade prostatic intraepithelial neoplasia) with striking nuclear atypia, and invasive poorly differentiated carcinoma. In mouse prostate organoids, mutant SPOP drove increased proliferation and a transcriptional signature consistent with human prostate cancer. Using these models and human prostate cancer samples, we show that SPOP mutation activates both PI3K/mTOR and androgen receptor (AR) signaling, effectively uncoupling the normal negative feedback between these two pathways. Associated RNA-seq data deposited in GEO: GSE94839.

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SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (BRDs_OE_RNA-seq)

Project description:Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. BET protein levels are highly elevated in SPOP-mutated prostate cancers in patients. Expression of cancer-derived SPOP mutants upregulates cholesterol biosynthesis genes and confers resistance to the BET inhibitor in cultured prostate cancer cells and tumors in mice, and this effect can be overcome by the AKT inhibitor. Our findings reveal BET proteins as proteolytic targets of SPOP and identify deregulated cholesterol biosynthesis as a downstream event of SPOP mutation-mediated tumorigenesis and therapy resistance in prostate cancer.

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