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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE165280 | GEO | 2022/04/01

REPOSITORIES: GEO

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ChIP-seq analysis of genome-edited MCF7 and T47D ESR1 mutant cell models

Project description:This study is designed to comprehensively characterize the cistromes of Y537S and D538G mutated ER versus WT ER in breast cancer cells. Genome-edited MCF7 and T47D cells were hormone deprived and treated with or without E2 for 45 minuts. Chromatin DNA was then extracted from each sample. The immunoprecipitation was performed using ERα (Santa Cruz Biotechnologies, sc543) antibody. Pooled DNA samples from individual clones were sent to sequencing with Illumina Hiseq 2500 Platform. ChIP-seq reads were aligned to either hg38 genome assembly using Bowtie 2.0, and peaks were called using MACS2.0 with p value below 10E-5. DiffBind was used to perform principle component analysis, identify differentially expressed binding sites and analyze intersection ratios with other data sets. Genomic feature distribution were called using ChIPseeker.

2021-01-01 | GSE125117 | GEO

RNA-seq analysis of ESR1 mutations in T47D and MCF7 cell lines

Project description:Purpose: Transcriptome analysis of ESR1 mutant cells was performed via sequencing total RNA in T47D and MCF7 cell lines containing Y537S and D538G mutations.

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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

Targeting ESR1 mutation-induced transcriptional addiction with BET inhibition

Project description:We investigated the therapeutic potential of BET inhibition to target ESR1 mutation-induced “transcriptional addiction” in ER-positive breast cancer. Our studies show that ESR1 mutant (Y537S and D538G) cells activate unique transcriptional programs that are targeted by OTX015, a BET inhibitor

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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.

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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

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

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

| PRJNA693859 | ENA

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

2013-10-25 | GSE51448 | GEO

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [RNA-Seq]

Project description:Estrogen receptor-Î± (ERÎ±) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. MCF-7-Y537S cells encode a wild-type (tyrosine 537) and a mutant (serine 537) allele. Growth of the line is estrogen-independent and expression of ERÎ± target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERÎ± binding sites in the presence and absence of estrogen. RNA-seq following estrogen treatment was used for gene expression analysis. We show that expression of ER target genes and ER recruitment to ER binding regions is similar in MCF-7 and MCF-7-Y537S cells, except that ER recruitment to DNA and expression of ER target genes is frequently elevated in the absence of estrogen. Hormone depleted MCF7 Luc or Y537S cells were treated with 10nM E2 or ethanol, as vehicle control, for 8 hours, with 3 replicates (2 replicates for Y537S + E2). RNA-seq was carried out using Illumina Hiseq 2500.

2016-10-25 | E-GEOD-78285 | biostudies-arrayexpress

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [ChIP-Seq]

Project description:Estrogen receptor-Î± (ERÎ±) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. MCF-7-Y537S cells encode a wild-type (tyrosine 537) and a mutant (serine 537) allele. Growth of the line is estrogen-independent and expression of ERÎ± target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERÎ± binding sites in the presence and absence of estrogen. RNA-seq following estrogen treatment was used for gene expression analysis. We show that expression of ER target genes and ER recruitment to ER binding regions is similar in MCF-7 and MCF-7-Y537S cells, except that ER recruitment to DNA and expression of ER target genes is frequently elevated in the absence of estrogen Hormone depleted MCF-7 LUC /Y537S mutant cells were treated with estrogen (10nM) or ETOH as vehicle control for 45 mins. ErÎ± Chip-seq was performed using Illumnia methodology

2016-10-25 | E-GEOD-78284 | biostudies-arrayexpress

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