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Genome-wide estrogen receptor-α binding and action in human endometrial stromal cells [RNA-Seq]

ABSTRACT: Genome-wide estrogen receptor-α binding and action in human endometrial stromal cells [RNA-Seq]

PROVIDER: PRJNA635669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11868511.fastq.gz	Fastqsanger.gz
	SRR11868512.fastq.gz	Fastqsanger.gz
	SRR11868513.fastq.gz	Fastqsanger.gz
	SRR11868514.fastq.gz	Fastqsanger.gz
	SRR11868515.fastq.gz	Fastqsanger.gz

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Genome-wide estrogen receptor-α binding and action in human endometrial stromal cells

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Genome-wide estrogen receptor-α binding and action in human endometrial stromal cells [RNA-Seq]

Project description:Endometrial estrogen receptor-α (ESR1) is indispensable for epithelial and stromal proliferation and differentiation during decidualization, yet the gene targets of estradiol (E2) / ESR1 in human stromal cells and associated mechanisms remain unknown. In this study, we characterized global E2-ESR1‒dependent transcriptomic changes and ESR1 recruitment to chromatin. Human endometrial stromal cells were isolated from 4 premenopausal women for primary cell culture. Genome-wide RNA expression by RNA-sequencing was compared in endometrial stromal cells with or without siRNA knockdown of ESR1 in the presence or absence of E2 (n=2). Genome-wide recruitment of ESR1 to chromatin was assessed by chromatin immunoprecipitation sequencing using an antibody against ESR1 was performed to examine binding to target genes (n=1).

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Expression data of differentially regulated genes in ESR1 depleted human endometrial stromal cells during differentiation.

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Project description:Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells.

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