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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE89888 | GEO | 2017/06/03

SECONDARY ACCESSION(S): PRJNA353646

REPOSITORIES: GEO

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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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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

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Project description:Estrogen receptor (ER) is the major driver of a large proportion of breast cancers, and many therapies have been designed to target it. These include anti-estrogens, which target ER directly, and aromatase inhibitors, which instead prevent the biosynthesis of estrogen in post-menopausal women. These therapies have been largely successful, but unfortunately many patients eventually succumb to resistance. A hotspot of mutations in exon 8 of ESR1, which cause the ER to be constitutively active, have been discovered in advanced breast cancer patients, and are one cause of resistance to aromatase inhibitors as well as a reduced response to anti-estrogen therapies. Since most studies in to these mutations have so far focused on the mostly commonly seen mutations, Y537S and D538G, it is important to extend our understanding to other frequently found mutations to determine whether there are intrinsic differences between them. For this purpose, CRISPR-Cas9 was used in order to model the following mutations found in exon 8 of ESR1 in breast cancer patients, L536R, Y537C, Y537S, Y537N and D538G, in MCF7 cells, with between two to four clones of each mutation generated. Growth in the absence of estrogen and in the presence of various SERDs was tested to investigate differences in sensitivity between mutations. RNA-seq was carried out in the ESR1 mutant MCF7 lines under full medium conditions to look for gene expression changes compared to WT, shared between all mutations, or the possibility of differences between specific mutations, which were not due to the fact that the ESR1 mutant lines can grow in the absence of estrogen. The results of which should provide great insight into potential alternative genes or pathways, which could be targeted in patients harbouring these mutations.

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