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

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

PROVIDER: PRJNA737452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14807787_1.fastq.gz	Fastqsanger.gz
	SRR14807787_2.fastq.gz	Fastqsanger.gz
	SRR14807788_1.fastq.gz	Fastqsanger.gz
	SRR14807788_2.fastq.gz	Fastqsanger.gz
	SRR14807789.fastq.gz	Fastqsanger.gz

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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

| PRJNA737445 | ENA

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

Project description:Uterine Leiomyomas (UL) are benign tumors that arise in the myometrium of the uterus. The standard treatment option for UL is hysterectomy but hormonal treatment options are emerging in the field. However, since the pathogenesis of UL is poorly understood, hallmarks that predict long-term efficacy and safety of these treatment options remain largely undefined. We have reported previously that REST/NRSF target genes are aberrantly expressed due to the near ubiquitous loss of this epigenetic repressor in UL tumors. We show that ablation of Rest in the mouse uterus leads to UL phenotype and altered response to steroid hormones estrogen and progesterone. Additionally, we demonstrate that a large number of REST target genes dysregulated in UL as well as in Rest cKO mice, are also targets of progesterone receptor (PR). Importantly, we identify a direct interaction between REST and PR in the healthy myometrium. Rest cKO mouse model phenocopies human UL, including gene expression profiles of UL as well as tumor formation in the myometrium. Our findings emphasize the critical role loss of REST plays in disease pathogenesis and the altered response to steroid hormones seen in UL.

2022-10-12 | GSE178140 | GEO

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

2022-10-12 | GSE178086 | GEO

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

Expression profiling of long noncoding RNAs and mRNAs in uterine leiomyoma

Project description:Global protein coding gene and miRNA expression profiling studies in uterine leiomyoma showed their aberrant expression and involvement in the pathogenesis of uterine leiomyoma. But the global expression patterns and potential clinical value of long noncoding RNA (lncRNA) in uterine leiomyoma have not been explored.In this study, we performed lncRNA expression profiles analysis of uterine leiomyoma using microarray(Arraystar Human LncRNA Array v2.0) to evaluate the genome-wide expression of lncRNAs and mRNAs and their potential role in the pathogenesis of uterine leiomyoma.

2014-08-14 | GSE52618 | GEO

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.

Project description:Uterine leiomyomas (UL) are benign tumors that arise in the myometrial layer of the uterus. The standard treatment option for UL is hysterectomy, although hormonal therapies, such as selective progesterone receptor modulators, are often used as temporary treatment options to reduce symptoms or to slow the growth of tumors. However, since the pathogenesis of UL is poorly understood and most hormonal therapies are not based on UL-specific, divergent hormone signaling pathways, hallmarks that predict long-term efficacy and safety of pharmacotherapies remain largely undefined. In a previous study, we reported that aberrant expression of repressor element 1 silencing transcription factor/neuron-restrictive silencing factor (REST/NRSF) target genes activate UL growth due to the near ubiquitous loss of REST. Here, we show that ablation of the Rest gene in mouse uterus leads to UL phenotype and gene-expression patterns analogous to UL, including altered estrogen and progesterone signaling pathways. We demonstrate that many of the genes dysregulated in UL harbor cis-regulatory elements bound by REST and progesterone receptor (PGR) adjacent to each other. Crucially, we identify an interaction between REST and PGR in healthy myometrium and present a putative mechanism for the dysregulation of progesterone-responsive genes in UL ensuing in the loss of REST. Using three Rest conditional knockout mouse lines, we provide a comprehensive picture of the impact loss of REST has in UL pathogenesis and in altering the response of UL to steroid hormones.

| S-EPMC9636955 | biostudies-literature

Expression profiling of long noncoding RNAs and mRNAs in uterine leiomyoma

2014-08-14 | E-GEOD-52618 | biostudies-arrayexpress

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

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

2012-09-11 | GSE40724 | GEO