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Transcriptomic profiling of MCF-7 breast cancer cells treated with G1, a G-protein coupled estrogen receptor (GPER1) agonist

ABSTRACT: Application of next generation sequencing (NGS) technology to identify G1-modulated genes in MCF-7 breast cancer cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE188706 | GEO | 2021/11/27

REPOSITORIES: GEO

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Transcriptomic profiling of MCF-7 breast cancer cells treated with G1, a G-protein coupled estrogen receptor (GPER1) agonist

Project description:Transcriptomic profiling of MCF-7 breast cancer cells treated with G1, a G-protein coupled estrogen receptor (GPER1) agonist

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Transcriptomic data of MCF-7 breast cancer cells treated with G1, a G-protein coupled estrogen receptor (GPER) agonist.

Project description:Besides short-term non-genomic effects, the G-protein coupled estrogen receptor (GPER) also mediates long-term genomic effects of estrogen. The genomic effects of GPER activation are not completely understood. G1 is a selective GPER agonist, which is popularly used for addressing the effects of GPER activation. Here, we present transcriptomic (RNA-seq) data on MCF-7 cells treated with 100 nM, or 1 µM G1 for a period of 48 h. The data are available from GEO (accession number GSE188706).

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Transcriptomic profiling of MCF-7 breast cancer cells treated with Karanjin

Project description:Application of next generation sequencing (NGS) technology to identify karanjin-modulated genes in MCF-7 breast cancer cells

2022-08-30 | GSE183913 | GEO

G-Protein-Coupled Estrogen Receptor (GPER)-Specific Agonist G1 Induces ER Stress Leading to Cell Death in MCF-7 Cells.

Project description:The G-protein-coupled estrogen receptor (GPER) mediates rapid non-genomic effects of estrogen. Although GPER is able to induce proliferation, it is down-regulated in breast, ovarian and colorectal cancer. During cancer progression, high expression levels of GPER are favorable for patients' survival. The GPER-specific agonist G1 leads to an inhibition of cell proliferation and an elevated level of intracellular calcium (Ca2+). The purpose of this study is to elucidate the mechanism of G1-induced cell death by focusing on the connection between G1-induced Ca2+ depletion and endoplasmic reticulum (ER) stress in the estrogen receptor positive breast cancer cell line MCF-7. We found that G1-induced ER Ca2+ efflux led to the activation of the unfolded protein response (UPR), indicated by the phosphorylation of IRE1α and PERK and the cleavage of ATF6. The pro-survival UPR signaling was activated via up-regulation of the ER chaperon protein GRP78 and translational attenuation indicated by eIF2-α phosphorylation. However, the accompanying pro-death UPR signaling is profoundly activated and responsible for ER stress-induced cell death. Mechanistically, PERK-phosphorylation-induced JNK-phosphorylation and IRE1α-phosphorylation, which further triggered CAMKII-phosphorylation, are both implicated in G1-induced cell death. Our study indicates that loss of ER Ca2+ is responsible for G1-induced cell death via the pro-death UPR signaling.

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Bisulfite sequencing coupled to target enrichment in MCF-7

Project description:Sequencing of bisulfite-converted MCF-7 genomic DNA captured on SureSelect Methyl-Seq (Agilent).

2017-10-19 | GSE69505 | GEO

Expression data of hormone-responsive MCF-7 cells versus estrogen-deprived MCF-7:5C and MCF-7:2A breast cancer cells

Project description:Estrogen deprivation using aromatase inhibitors is currently the standard of care for patients with estrogen-receptor (ER)-positive breast cancer. Unfortunately, prolonged estrogen deprivation leads to drug resistance (i.e. hormone-independent growth). We therefore used DNA microarray analysis to study the gene expression profiles of wild-type MCF-7 cells (which are sensitive to antihormone therapy) and long-term estrogen deprived MCF-7:5C and MCF-7:2A breast cancer cells (which are resistance to estrogen-deprivation; aromatase inhibitor resistant). Transcriptional profiling of wild-type MCF-7 cells and estrogen deprived MCF-7:5C and MCF-7:2A cells was performed using Affymetrix Human Genome U133 Plus 2.0 Array. Keywords: breast cancer cells, estrogen

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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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Shouchella lehensis G1 strain:G1

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G Protein-Coupled Estrogen Receptor 1 (GPER1) Mediates Aldosterone-Induced Endothelial Inflammation in a Mineralocorticoid Receptor-Independent Manner.

Project description:ObjectiveIt has been increasingly appreciated that G protein-coupled estrogen receptor 1 (GPER1) mediates both proinflammatory and anti-inflammatory response of estrogen. It is also involved in some rapid vascular effects of aldosterone in a mineralocorticoid receptor (MR) independent manner. However, whether GPER1 mediates aldosterone-induced inflammation response in endothelial cells and its relationship with MR are yet undetermined and therefore require further explanation.MethodBased on the hypothesis that GPER1 plays a role in the aldosterone-related vascular inflammation, the present study utilized a model of human umbilical vein endothelial cells transfected with MR siRNA and induced for inflammatory response with increasing concentration of aldosterone.ResultsIt was discovered that induction of aldosterone had no effect on the expression of GPER1 but promoted the expression of MR. Suppression of MR did not influence GPER1 expression, and GPER1 was capable of mediating part of aldosterone-induced endothelial inflammatory response. This effect may involve phosphoinositide 3-kinases (PI3K) pathway signaling.ConclusionThese findings not only demonstrated the role of GPER1 in aldosterone-induced vascular inflammation but also suggested an alternative for pharmaceutical treatment of hyperaldosteronism considering the unsatisfying effect on cardiovascular risks with MR antagonists.

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Genome-wide effects of enterolactone on gene expression in MCF-7 cells

Project description:Application of next generation sequencing technology to identify genes modulated by enterolactone in MCF-7 cells

2023-01-06 | GSE216876 | GEO