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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [RNA-Seq]

ABSTRACT: Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [RNA-Seq]

PROVIDER: PRJNA546515 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9202890.fastq.gz	Fastqsanger.gz
	SRR9202891.fastq.gz	Fastqsanger.gz
	SRR9202882.fastq.gz	Fastqsanger.gz
	SRR9202892.fastq.gz	Fastqsanger.gz
	SRR9202883.fastq.gz	Fastqsanger.gz

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [methylArray]

Project description:Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER) orchestrates a complex molecular circuitry that is not yet fully elucidated. Here we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression. Enrichment analysis of transcription factor (TF) binding and motif occurrence in the proximity of E2 deprivation-mediated differentially methylated and acetylated sites reinforces the importance of AP-1 and FOX proteins, Finally, most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation.

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation

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2020-01-01 | GSE132510 | GEO

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [methylArray]

Project description:Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [methylArray]

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [ChIP-Seq]

Project description:Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [ChIP-Seq]

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation.

Project description:Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER), the main nuclear factor mediating estrogen signaling, orchestrates a complex molecular circuitry that is not yet fully elucidated. Here, we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterize the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression, and more specifically of TET2 demethylase that may be involved in the DNA hypermethylation following short-term E2 deprivation. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER connection mainly with two partner TF families, AP-1 and FOX. These interactions take place in the proximity of E2 deprivation-mediated differentially methylated and histone acetylated enhancers. Finally, while most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation, DNA hypermethylation and H3K27 deacetylation at certain enhancers were partially retained. Overall, these results show that inactivation of ER mediates rapid and mostly reversible epigenetic changes at enhancers, and bring new insight into early events, which may ultimately lead to endocrine resistance.

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Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation

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

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miRNA expression profiles of estrogen-dependent and estrogen deprivation-resistant MCF-7 breast cancer cell lines

Project description:A series of MCF-7 variants were previously developed that are estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation/vulnerable to fast (MCF-7:5C) and delayed (MCF-7:2A) E2-inducible apoptosis. To identify miRNAs associated with aromatase inhibitor (AI)-resistance and vulnerability to E2-induced apoptosis, estrogen deprivation-resistant 5C and 2A cells were compared to estrogen-dependent WS8 cells and among each other.

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Project description:A series of MCF-7 variants were previously developed that are either estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation and refractory (MCF-7:2A) or sensitive (MCF-7:5C) to E2-induced apoptosis. To identify genes associated with E2-induced apoptosis, estrogen deprivation-resistant/apoptotic-sensitive 5C cells were compared to both estrogen-dependent MCF-7:WS8 and estrogen deprivation/apoptotic-refractory MCF-7:2A cells

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