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E-MTAB-5537

ABSTRACT: RNA-seq of the human breast cancer ER-suppressed MCF-7(MCF-7/SP10+) cells and of their internal control MCF-7 (MCF-7/C) cells

PROVIDER: E-MTAB-5537 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-5537-analysis-methods.tsv	Tabular
	E-MTAB-5537-analytics.tsv	Tabular
	E-MTAB-5537-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-5537-configuration.xml	Xml
	E-MTAB-5537-g2_g1-mvaPlot.png	Other

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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

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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

RNA-seq of the human breast cancer ERα-suppressed MCF-7(MCF-7/SP10+) cells and of their internal control MCF-7 (MCF-7/C) cells

Project description:RNA-seq of the human breast cancer ERα-suppressed MCF-7(MCF-7/SP10+) cells and of their internal control MCF-7 (MCF-7/C) cells

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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-α (ERα) 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 ERα target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERα 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

2016-10-25 | GSE78284 | GEO

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MicroRNAs expression data from two different types of human breast cancer cells

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