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Homo sapiens

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

PROVIDER: PRJNA353646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5024090_1.fastq.gz	Fastqsanger.gz
	SRR5024090_2.fastq.gz	Fastqsanger.gz
	SRR5024100_1.fastq.gz	Fastqsanger.gz
	SRR5024100_2.fastq.gz	Fastqsanger.gz
	SRR5024110_1.fastq.gz	Fastqsanger.gz

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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.

2017-06-03 | GSE89888 | GEO

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 (RNA-seq)

2021-10-19 | GSE159802 | GEO

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

2021-10-21 | GSE159724 | GEO

Transcriptional reprogramming underpinning resistance to endocrine therapy and CDK4/6 inhibitors in ER+ breast cancer cell lines

Project description:To investigate the molecular mechanisms of resistance to ER downregulator and CDK4/6 inhibitors in ER+ breast cancer, we generated two cell lines, MCF7 and T47D, resistant to fulvestrant and abemaciclib after 6-8 months of exposure to increasing doses of the drug combination We performed gene expression profiling analysis using data obtained from RNA-seq of parental MCF7 or T47D and the respective fulvestrant and abemaciclib resistant cells

2023-06-05 | GSE227102 | GEO

Discovery of naturally occurring ESR1 mutations during acquisition of resistance to endocrine therapy in widely used estrogen receptor positive breast cancer cell lines [ChIP-Seq]

Project description:We report the first discovery of naturally occurring ESR1Y537C and ESR1Y537S mutations in MCF7 and MCF7 ESR1-positive cell-lines after acquisition of resistance to long-term-estrogen-deprivation (LTED) and subsequent resistance to fulvestrant (ICIR).

2018-01-12 | GSE100074 | GEO

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

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

| PRJNA515270 | ENA

TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells [ChIP-seq]

Project description:We report the ChIP-Seq profiles for TRPS1 and TEAD1 in MCF7 and T47D cell lines, and for YAP in MCF7 cells.

2018-08-07 | GSE107013 | GEO

RNA-seq of human breast cancer cell lines MCF7 and T74D naive and resistant to palbociclib treated with capivasertib, fulvestrant and combination

Project description:T47D and MCF7 cell lines were treated with long-term (continuous) palbociclib to induce 4 resistant cell-lines (T47D RB-, T47D CDK6H, MCF7 RB- and MCF7 PacqR). Each cell line (both parental and resistant) were then treated with DMSO (control), capivasertib monotherapy, fulvestrant monotherapy and capivasertib/fulvestrant combination. RNA data is available after each treatment and resistant cell lines additionally have RNA data available after continuous palbociclib treatment.

2023-08-14 | E-MTAB-13262 | 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

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