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DNA methylome regulation by progesterone receptor in primary leiomyoma cells

ABSTRACT: DNA methylome regulation by progesterone receptor in primary leiomyoma cells

PROVIDER: PRJNA623613 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11504916.fastq.gz	Fastqsanger.gz
	SRR11504917.fastq.gz	Fastqsanger.gz
	SRR11504918.fastq.gz	Fastqsanger.gz
	SRR11504919.fastq.gz	Fastqsanger.gz
	SRR11504920.fastq.gz	Fastqsanger.gz

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Genome-wide transcriptome regulation by progesterone receptor in primary leiomyoma cells

Project description:Genome-wide transcriptome regulation by progesterone receptor in primary leiomyoma cells

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DNA methylome regulation by progesterone receptor in primary leiomyoma cells

Project description:Uterine leiomyomas (LM) affect up to 80% of all reproductive-age women. LM growth requires progesterone, progesterone receptor (PGR), and the maintenance and proliferation of a small (5%) stem cell population. Stem cell activation and differentiation are driven by DNA methylation and nuclear hormone receptor action, but crosstalk between these mechanisms remains unclear. We performed an integrated analysis of the transcriptome and epigenetic landscape of LM cells at three differentiation stages and the PGR cistrome of whole LM tissue. The PGR-deficient stem cell population harbored a unique methylation landscape, with hypermethylation at the PGR gene locus and PGR-binding regions, which suppressed stem cell responsiveness to progesterone. The DNA methylation inhibitor 5’-Aza upregulated the expression of PGR and its target genes by stimulating PGR recruitment to the targeted gene loci, and significantly depleted the LM stem cell population and its tumor-initiating capacity. We herein provided mechanistic insights via therapeutically accelerating the stem cell differentiation process of a hormone-sensitive tumor.

2021-08-01 | GSE148256 | GEO

Genome-wide transcriptome regulation by progesterone receptor in primary leiomyoma cells

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Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis

Project description:Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis

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Progesterone receptor signaling is inhibited by hypermethylation in leiomyoma stem cells to maintain stemness

Project description:Progesterone receptor signaling is inhibited by hypermethylation in leiomyoma stem cells to maintain stemness

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Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (ChIP-Seq)

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. We applied ChIP-seq to identify PR-interaction sites in T47D breast cancer cells and primary uterine leiomyoma cells treated with RU486.

2012-09-11 | E-GEOD-40724 | biostudies-arrayexpress

Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis [RNA-seq]

Project description:Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis [RNA-seq]

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Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis [scRNA-seq]

Project description:Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis [scRNA-seq]

| PRJNA737342 | ENA

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (ChIP-Seq)

2012-09-11 | GSE40724 | GEO

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. Total RNA isolated from T47D cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells. Total RNA isolated from uterine leiomyoma cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells.

2011-07-22 | E-GEOD-30871 | biostudies-arrayexpress

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