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ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [RNA-seq]

ABSTRACT: ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [RNA-seq]

PROVIDER: PRJNA475140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7277690_1.fastq.gz	Fastqsanger.gz
	SRR7277690_2.fastq.gz	Fastqsanger.gz
	SRR7277686_1.fastq.gz	Fastqsanger.gz
	SRR7277686_2.fastq.gz	Fastqsanger.gz
	SRR7277687_1.fastq.gz	Fastqsanger.gz

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ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity

Project description:ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity

| PRJNA476796 | ENA

ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [ChIP-seq]

Project description:Deficiency in homologous recombination repair (HRR) is frequently associated with hormone-responsive cancers. Epithelial ovarian cancer (EOC) is a typical hormone-related tumor, with defects of HRR in up to half of cases. However, whether there are molecular connections between estrogen signaling and HRR deficiency in EOC remains unknown. Here we report an inverse correlation between estrogen signaling and HRR activity in EOC. Genome-wide mapping of ERα reveals ERα co-bindings with co-repressor CtBP, especially on many HRR gene loci, in EOC cells but not in breast cancer cells. Consistently, depleting ERα in EOC cells up-regulates HRR activity and HRR gene expression. Importantly, estrogen signaling enhances the sensitivity of ovarian cancer cells to chemotherapy agents in vitro and in vivo. Large-scale analyses further indicate that estrogen replacement and ERα expression are associated with favorable survival of EOC patients. These findings characterize a novel role of ERα in mediating the molecular connection between hormone and HRR in EOC, and suggest that estrogen signaling may improve the treatment outcome of EOC patients.

2019-06-26 | GSE116005 | GEO

ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [RNA-seq]

2019-06-26 | GSE115481 | GEO

ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [ChIP-seq]

Project description:ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity [ChIP-seq]

| PRJNA476785 | ENA

ERα-CtBP-mediated repression of Homologous-recombination repair in ovarian cancer improves chemo-sensitivity

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

2019-06-26 | GSE116018 | GEO

Three-dimensional Oxabicycloheptene sulfonate targets the homologous recombination and repair programs through estrogen receptor α antagonism

Project description:Selective Estrogen Receptor Modulators (SERMs) are a class of structurally diverse compounds possessing unique partially agonistic and antagonistic properties and have been extensively used in treatments of hormone-responsive cancers and other diseases. Our previous studies have identified a three-dimensional SERM oxabicycloheptene sulfonate (OBHS) for estrogen receptor α (ERα), which is effective in vivo for the prevention and treatment of estrogen-dependent endometriosis. Here, using ChIP-seq and RNA-seq analysis, we found that OBHS rapidly induces genome-wide ERα occupancy behaves as a partial agonist and antagonist in ERα positive MCF-7 cells. Interestingly, OBHS downregulates the homologous recombination and repair (HRR) modules resulting in the increased DNA damage, apoptosis and cell cycle arrest, and leading to synthetic lethality with Poly (ADP-ribose) polymerase (PARP) inhibitor olaparib and genotoxic doxorubicin through blocking of ERα. Furthermore, we found that OBHS treatment results in defects of RNA polymerase II loading at the estrogen-responsive HRR genes, providing a mechanism for the regulation of HRR genes by OBHS. Together, our studies not only reveal a novel SERM OBHS which uniquely targets the homologous recombination and repair programs through ERα antagonism, but also propose a synthetic lethal strategy by combining OBHS with PARP inhibitor olaparib or genotoxic doxorubicin for ERα-responsive cancers.

2019-12-20 | GSE133941 | GEO

Expression data from CtBP knockdown MCF-7 cells

Project description:CtBP is a global co-repressor by serving as transcriptional factor in multiple pathways. CtBP functioned as transcriptional factor by recruiting other cofactors such as G9a, HDAC1 and PcG proteins. CtBP is found to be over enriched in several type of tumor samples. To dipict the role of CtBP in globally regulating gene expression, we applied gene microarray technology to find out what subgroups of genes are mainly affected. 6 MCF-7 cell samples, 3 with CtBP knockdown and 3 with control knock down.

2013-03-20 | E-GEOD-36529 | biostudies-arrayexpress

Expression data from CtBP knockdown MCF-7 cells

2013-03-20 | GSE36529 | GEO

Genome-wide maps of CtBP binding profile in breast cancer cell line MCF-7

Project description:CtBP is a global co-repressor by serving as transcriptional factor in multiple pathways. CtBP functioned as transcriptional factor by recruiting other cofactors such as G9a, HDAC1 and PcG proteins. CtBP is found to be over enriched in several type of tumor samples. To dipict the role of CtBP in globally regulating gene expression, we applied ChIP-seq technology to find out the binding profile of CtBP in breast cancer cell line MCF-7. Our data suggest CtBP plays a global regulatory role in DNA damage repair, tumor initiation, and EMT process. Examine CtBP binding in MCF-7 cells

2013-03-20 | E-GEOD-36546 | biostudies-arrayexpress

Genome-wide maps of CtBP binding profile in breast cancer cell line MCF-7

Project description:CtBP is a global co-repressor by serving as transcriptional factor in multiple pathways. CtBP functioned as transcriptional factor by recruiting other cofactors such as G9a, HDAC1 and PcG proteins. CtBP is found to be over enriched in several type of tumor samples. To dipict the role of CtBP in globally regulating gene expression, we applied ChIP-seq technology to find out the binding profile of CtBP in breast cancer cell line MCF-7. Our data suggest CtBP plays a global regulatory role in DNA damage repair, tumor initiation, and EMT process.

2013-03-20 | GSE36546 | GEO

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