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Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells

ABSTRACT: Analysis of MCF7 cells transfected with ER mutants (S463P, Y537S and D538G) in phenol-red free, charcoal stripped FBS media and regular DMEM/F12 media. Results provide insight on the gene expression profiles induced by the various ER mutants. Total RNA extracted from transfected cells 48 hours after transfection

ORGANISM(S): Homo sapiens

PROVIDER: GSE51448 | GEO | 2013/10/25

SECONDARY ACCESSION(S): PRJNA223675

REPOSITORIES: GEO

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Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells

Project description:Analysis of MCF7 cells transfected with ER mutants (S463P, Y537S and D538G) in phenol-red free, charcoal stripped FBS media and regular DMEM/F12 media. Results provide insight on the gene expression profiles induced by the various ER mutants. Total RNA extracted from transfected cells 48 hours after transfection 36 samples were analyzed, triplicates for each constructs (GFP vector control, WT, S463P, Y537S, D538G and S463P/D538G) for each type of media

2013-10-25 | E-GEOD-51448 | biostudies-arrayexpress

ESR1 Y537S and D538G mutations drive resistance to CDK4/6 inhibitors in estrogen receptor-positive breast cancer

Project description:Purpose: Breast cancers with ESR1 mutations are resistant to antiestrogen therapy. We aimed to investigate the association of ESR1 mutations with resistance to CDK4/6 inhibitors (CDK4/6i) using real-world data analysis and experimental validation. Patients and Methods: A total of 3,958 patients with estrogen receptor-positive (ER+) metastatic breast cancer with DNA sequencing data were analyzed. Breast tumor DNA and circulating tumor (ct) DNA were sequenced using the Tempus xT tumor assay and Tempus xF liquid biopsy, respectively. Patients were stratified into either treated with CDK4/6i (breast tumors: 1,070; ctDNA: 1,885) or CDK4/6i naïve (breast tumors: 750; ctDNA: 253). Engineered MCF7 cells carrying ESR1 Y537S or D538G knock-in mutations were used to study antitumor efficacy of the CDK4/6i, palbociclib in vitro and in vivo. Results: In both xF and xT assays, ESR1 mutations were the only somatic alterations significantly more frequent in those who received CDK4/6i than those who did not. Knock-in of ESR1 Y537S or ESR1 D538G in MCF7 cells resulted in upregulation of cell cycle-related gene signatures upon treatment with CDK4/6i ± antiestrogen compared to cells with non-mutant ESR1. MCF7 xenografts harboring ESR1 Y537S and D538G mutations established in nude mice were resistant to palbociclib. Conclusions: We report herein real-world and preclinical evidence that ESR1 mutations, particularly Y537S and D538G, can drive resistance to CDK4/6 inhibitors.

2024-11-12 | GSE281302 | GEO

FOXA1 ChIP-seq analysis of genome-edited T47D ESR1 mutant cell models

Project description:This study is designed to comprehensively characterize the FOXA1 cistromes of Y537S and D538G mutated ER versus WT ER in breast cancer cells.

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H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

Project description:H3K27Ac ChIP-seq in MCF7 Y537S ER mutant cells RNAseq analysis of MCF7 Y537S ER mutant cells treated with veh and THZ1

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Project description:To investigate the effect of diptoindonesin G on breast cancer cells expressing the estrogen receptor Y537S ligand binding domain mutation, we treated T47D cells overexpressing the ER Y537S mutation and treated them with vehicle or diptoindonesin G and performed differential gene expression analysis and gene set enrichment analysis

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Targeting ESR1 mutation-induced transcriptional addiction with BET inhibition

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Estrogen Receptor Mutant Coregulator

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RNAseq of cell lines with knocked in ESR1 mutations

Project description:The study was designed to investigae the transcriprional changes induced by the Y537S, D538G and E380Q ESR1 mutations

2019-03-22 | GSE112243 | GEO

Genome-wide analysis of transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

Project description:We analyzed the chromatin state of MDA-MB-453 cells expressing wild-type, Y537S, or K303R ER alpha by ATAC-seq, and identified K303R-related disordered chromatin opening which has Fox-binding motifs.

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Time-course effect of estradiol and estradiol-BSA on early gene expression in MCF-7 cells

Project description:Estrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor. Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with or without E2-BSA (10-6M) in the presence or absence of specific antagonists, in DMEM/F12 (1:1) supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.

2012-01-01 | E-GEOD-32667 | biostudies-arrayexpress

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