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

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

PROVIDER: PRJNA623607 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10189631.fastq.gz	Fastqsanger.gz
	SRR10189632.fastq.gz	Fastqsanger.gz
	SRR10189633.fastq.gz	Fastqsanger.gz
	SRR10189634.fastq.gz	Fastqsanger.gz
	SRR10189635.fastq.gz	Fastqsanger.gz

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

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

2021-08-01 | GSE148257 | GEO

DNA methylome regulation by progesterone receptor in primary leiomyoma cells

Project description:DNA methylome regulation by progesterone receptor in primary leiomyoma cells

| PRJNA623613 | ENA

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

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

| PRJNA574343 | ENA

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

2021-08-01 | GSE138050 | GEO

Relationship between Genome-Wide DNA Methylation and Gene Expression in Uterine Leiomyoma

Project description:Uterine leiomyomas, or fibroids, represent the most common benign tumor of the female reproductive tract. Fibroids become symptomatic in 30% of all women and up to 70% of African American women of reproductive age. Epigenetic dysregulation of individual genes has been demonstrated in leiomyoma cells; however, the in vivo genome-wide distribution of such epigenetic abnormalities, however, remains unknown. Principal Findings: We characterized and compared genome-wide DNA methylation and mRNA expression profiles in uterine leiomyoma and matched adjacent normal myometrial tissues from 18 African-American women. We found 55 genes with differential promoter methylation and concominant differences in mRNA expression in uterine leiomyoma versus normal myometrium. Eighty percent of the identified genes showed an inverse relationship DNA methylation status and mRNA expression in uterine leiomyoma tissues, and the majority of genes (62%) displayed hypermethylation associated with gene silencing. We selected two genes, the known tumor suppressors KLF11 and DLEC1, and verified promoter hypermethylation and mRNA repression using bisulfite sequencing and real-time PCR. Incubation of primary leiomyoma smooth muscle cells with a DNA methyltransferase inhibitor restored KLF11 and DLEC1 mRNA levels. paired LM and MM tissue samples

2012-04-29 | E-GEOD-31699 | biostudies-arrayexpress

Relationship between Genome-Wide DNA Methylation and Gene Expression in Uterine Leiomyoma

2012-04-30 | GSE31699 | GEO

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

| PRJNA737445 | ENA

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

Epigenome analysis of uterin leiomyoma and myometrium with or without leiomyoma [Methylation data]

Project description:Profiles of genome-wide DNA methylation were investigated in leiomyomas and in myometrium with and without leiomyomas. Profiles of DNA methylation in the myometrium with and without leiomyomas were quite similar while those in leiomyomas were distinct. Bisulphite converted DNA from the three uterine leiomyoma, three myometrium with leiomyoma and three myometrium without leiomyoma were hybridised to the Illumina infinium HumanMethylation450 BeadChip.

2013-09-01 | E-GEOD-45187 | biostudies-arrayexpress

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