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E-GEOD-41405

ABSTRACT: Genes affected by Ret activation during estrogen stimulation or inhibition in MCF7/Aro cells

OTHER RELATED OMICS DATASETS IN: PRJNA176962

PROVIDER: E-GEOD-41405 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-41405-analysis-methods.tsv	Tabular
	E-GEOD-41405-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-41405-configuration.xml	Xml
	E-GEOD-41405-percentile-ranks.tsv	Tabular
	E-GEOD-41405.condensed-sdrf.tsv	Tabular

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Project description:Genes affected by Ret activation during estrogen stimulation or inhibition in MCF7/Aro cells

| PRJNA176962 | ENA

Heat Shock Factor 1 (HSF1) regulates ESR1 action in breast cancer

Project description:Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. RNA-seq analyses revealed that the stimulatory effect of E2 on the transcriptome was smaller in HSF1-deficient MCF7 cells. This could partially result from the higher basal expression of E2-dependent genes in these cells as a consequence of the enhanced binding of unliganded ESR1 to chromatin, which was revealed by ChIP-seq analyses. Thus, we postulate that some fraction of ESR1 could be released from the inhibitory complex with HSP90 and gain transcriptional competence without E2-stimulation.

2021-12-18 | GSE186004 | GEO

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (ChIP-seq)

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Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (RNA-seq)

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A genomic view of estrogen actions in human breast cancer cells

Project description:Changes in the expression of 8400 genes were monitored by cDNA microarray analysis during the first 32 h of human breast cancer (BC) ZR-75.1 cell stimulation with a mitogenic dose of 17beta-estradiol, a timing which corresponds to completion of a full mitotic cycle in hormone-stimulated cells. Hierarchical clustering of 344 genes whose expression either increases or decreases significantly in response to estrogen reveals that the gene expression program activated by the hormone in these cells shows 8 main patterns of gene activation/inhibition. This newly identified estrogen-responsive transcriptome represents more than a simple cell cycle response, as only a few affected genes belong to the transcriptional program of the cell division cycle of eukaryotes, or showed a similar expression profile in other mitogen-stimulated human cells. Indeed, based on the functions assigned to the products of the genes they control, estrogen appears to affect several key features of BC cells, including their metabolic status, proliferation, survival, differentiation and resistance to stress and chemotherapy, as well as RNA and protein synthesis, maturation and turn-over rates. Keywords: time-course

2004-10-27 | GSE1864 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ATAC-seq]

Project description:We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in quadruplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.

2023-09-15 | GSE210603 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 2]

Project description:We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2, estrogen cepetor (ER) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and a specific ER-protac or vehicle was added for 24h for ER degradation. The day after, estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in duplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ER ChIP-seq]

Project description:We performed genome-wide mapping of estrogen receptor (ER) binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation upon metastasic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that E2 induces extensive ER recruitment to chromatin and that ER-binding is gained and expanded upon MAF overexpression.

2023-09-15 | GSE210604 | GEO

Expression data from MCF7 cells depleted of the cohesin subunit RAD21 and treated with estrogen or vehicle

Project description:RAD21 is a subunit of cohesin. Cohesin is maninly known for its role in holding sister chromatids together during cell-division but it also plays a role in gene regulation. Genome wide study in MCF7 cells have shown that cohesin co-binds with estrogen receptor alpha at numerous sites. To identify estrogen sensitive genes that are influenced by cohesin, a microarray expression analysis was conducted in MCF7 cells lacking the cohesin subunit RAD21. Global changes in gene expression were identified in cells treated with Control/RAD21 siRNA and stimulated with estrogen/vehicle thereafter.

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Chromatin binding alteration after enzalutamide treatment

Project description:In this study, we found the efficacy of AR-targeting drugs largely depended on the context of AR (Androgen Receptor) and ERα (Estrogen Receptor) status. Enzalutamide, an AR blocker, had a better inhibition effect on ER+ cells with lower AR expressed compared to cells expressed higher AR. To explore the mechanism of action of Enzalutamide, we performed ChIP-seq to illustrate the AR and ER genomic bindings after Enzalutamide treatment in both MCF7 and MCF7 with AR over expression (AROE) cells. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for androgen receptor (AR) and Estrogen receptor (ER) after Enzalutamide treatment in MCF7 and MCF7 AROE cells

2022-11-28 | GSE200300 | GEO

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