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Estrogen deprivation triggers and immunosuppressive phenotype in breast cancer cells

ABSTRACT: Estrogen deprivation triggers and immunosuppressive phenotype in breast cancer cells

PROVIDER: PRJNA556857 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9843460.fastq.gz	Fastqsanger.gz
	SRR9843461.fastq.gz	Fastqsanger.gz
	SRR9843462.fastq.gz	Fastqsanger.gz
	SRR9843463.fastq.gz	Fastqsanger.gz
	SRR9843464.fastq.gz	Fastqsanger.gz

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Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

Project description:Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

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Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells.

Project description:Among others, expression levels of programmed cell death 1 ligand 1 (PD-L1) have been explored as biomarkers of the response to immune checkpoint inhibitors in cancer therapy. Here, we present the results of a chemical screen that interrogated how medically approved drugs influence PD-L1 expression. As expected, corticosteroids and inhibitors of Janus kinases were among the top PD-L1 downregulators. In addition, we identified that PD-L1 expression is induced by antiestrogenic compounds. Transcriptomic analyses indicate that chronic estrogen receptor alpha (ERα) inhibition triggers a broad immunosuppressive program in ER-positive breast cancer cells, which is subsequent to their growth arrest and involves the activation of multiple immune checkpoints together with the silencing of the antigen-presenting machinery. Accordingly, estrogen-deprived MCF7 cells are resistant to T-cell-mediated cell killing, in a manner that is independent of PD-L1, but which is reverted by estradiol. Our study reveals that while antiestrogen therapies efficiently limit the growth of ER-positive breast cancer cells, they concomitantly trigger a transcriptional program that favors their immune evasion.

| S-EPMC8732350 | biostudies-literature

Estrogen deprivation triggers and immunosuppressive phenotype in breast cancer cells

Project description:Our study reveals that while antiestrogen therapies effectively limit tumor growth in ER-positive breast cancers, they also trigger a transcriptional program that favors immune evasion.

2019-07-27 | GSE134938 | GEO

Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells

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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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17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

2011-11-21 | GSE29917 | GEO

17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

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 Each cell line was treated with 10-9 M E2 or vehicle control over a 96 h time course consisting of 7 time points (2, 6, 12, 24, 48, 72 and 96 h) using 6 biological replicates per condition. cRNA probes from individual E2-treated samples were competitively hybridized against time-matched pooled control probes using 2-color Agilent 4x44k human oligonucleotide microarrays.

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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 [ChIP-Seq]

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

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