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Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

ABSTRACT: Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

PROVIDER: PRJNA558467 | ENA |

REPOSITORIES: ENA

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Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

Project description:Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

| PRJNA558468 | ENA

Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

Project description:Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

| PRJNA558466 | ENA

Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

Project description:Estrogen receptor alpha (ERα) signaling mainly occupies on distal enhancers within genome and plays an essential role in ERα-positive breast cancer. ERα usually requires co-factors to regulate the enhancer activity. By analysis of genome-wide nascent transcript profiling in breast cancer cells, we identified a special group of eRNAs that are functionally important for estrogen-induced transcriptional repression. In addition to stabilizing promoter-enhancer looping structure, these eRNAs recruit ERα to particular enhancers of target genes, facilitate the hierarchical formation of a functional transcriptional complex, and cause gene silencing. Interestingly, we found that ERα directly binds to eRNAs and its DNA-binding domain mediates the interaction with RNA molecules. Our ChIP-seq data in MCF-7 cells indicating that ERαwas not able to bind to E2-activated enhancers, which is consistent with the DNA-binding function reported before; moreover the DBD-truncated ERα was not able to bind to E2-repressed enhancers as well, which further supports our hypothesis that eRNA from E2-repressed enhancers help to recruit ERα to specific enhancers through the interaction with DBD domain. Substitution of ERα-DDBD showed a global effect on both induction and repression of ERα target genes as examined by RNA-seq. Further, these eRNAs help with the formation of a specific ERα-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses transcription of target genes. Our work demonstrated that eRNAs, as a distinctive class of cis-acting molecules besides chromatin regulatory elements, play an important role in modulating and refining locus-specific transcriptional program.

2020-06-23 | GSE135339 | GEO

Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

2020-06-23 | GSE135340 | GEO

Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor.

Project description:The function of enhancer RNAs (eRNAs) in transcriptional regulation remains obscure. By analyzing the genome-wide nascent transcript profiles in breast cancer cells, we identify a special group of eRNAs that are essential for estrogen-induced transcriptional repression. Using eRNAs of TM4SF1 and EFEMP1 as the paradigms, we find that these RNA molecules not only stabilize promoter-enhancer interactions but also recruit liganded estrogen receptor α (ERα) to particular enhancer regions, facilitate the formation of a functional transcriptional complex, and cause gene silencing. Interestingly, ERα is shown to directly bind with eRNAs by its DNA-binding domain. These eRNAs help with the formation of a specific ERα-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes. Our work demonstrates a complete mechanism underlying the action of eRNAs in modulating and refining the locus-specific transcriptional program.

| S-EPMC8564762 | biostudies-literature

Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

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

2020-06-23 | GSE135341 | GEO

Discovery of Selective Estrogen Receptor Covalent Antagonists (SERCAs) for the treatment of ERa(WT) and ERa(MUT) breast cancer.

Project description:Discovery of Selective Estrogen Receptor Covalent Antagonists (SERCAs) for the treatment of ERa(WT) and ERa(MUT) breast cancer.

| PRJNA475560 | ENA

Estradiol Induced Transcriptional Profile of EAAE DNA Binding Deficient ERa Uterus

Project description:To evaluate the ability of a DNA binding deficient ERa to mediate transcriptional responses in the mouse uterus, ovariectomized mice were injected with 100 ul of saline or 250 ng of estradiol (E2) in 100 ul saline, uterine tissue was collected 2 hours filllowing the injection, and RNA was isolated

2015-03-24 | GSE56423 | GEO

RAC1 is an essential cofactor for estrogen receptor alpha [ChIP-seq]

Project description:We identified a small GTPase protein RAC1 as an intrinsic cofactor in the estrogen receptor alpha (ER) complex that is required for the function of ER.

2021-08-09 | GSE169073 | GEO

ChIP-seq experiments of Estrogen Receptor Alpha (ERa) in the human breast cancer cell line T47D stably expressing GFP or neoGATA3

Project description:In this study, we investigated the functions of the most common GATA3 mutation (X308_Splice) that we called “neoGATA3”. Analysis of available molecular data from >3000 breast cancer patients revealed a dysregulation of the ERa-dependent transcriptional response in tumors carrying this mutations. ChIP-Seq analysis indicated that ERa binding is reduced in neoGATA3-expressing cells, especially at distal regions, suggesting that neoGATA3 interferes with the fine-tuning of ERa-dependent gene expression.

2020-06-29 | E-MTAB-9121 | biostudies-arrayexpress

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