ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
ChIP-seq predicted estrogen receptor biding sites in human breast cancer cell line MCF7.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 5 citations in OpenAlex.
- Estradiol and the Development of the Cerebral Cortex: An Unexpected Role?Frontiers in neuroscience · 2018Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to find estrogen receptor (ER) binding sites of estradiol (E2)-treated and control groups and discuss the roles of ER activation in the tumorigenesis and progression of various human cancers. The ER ChIP-seq data GSE19013 was downloaded from Gene Expression Omnibus database, including E2-treated data GSM470419 and control data GSM470418. MACS software was utilized to identify ER binding sites in two groups. R's ChIPpeakAnno was used to detect ER-regulated target genes. Motif finding was employed to analyze ER concordant transcription factors (TFs) in MCF7 cell. The Gene Ontology (GO) was used to conduct functional enrichment analysis. We identified 9,134 ER binding sites in E2 stimulation group and 1,969 in control group. GO enrichment analysis of target genes showed that ER-regulated target genes mainly participated in mRNA catabolic process, protein complex disassembly, and protein localization to organelle-related biology process; while in E2 stimulation group, the function of ER-regulated target genes sharply changed. The effect of E2 in MCF7 cell suggested that activated ER probably reacted with several TFs and then co-regulated related genes expression. Furthermore, several TFs, such as PAX6, SMAD3, and ESR2, had multiply cellular regulation function. Our results showed that E2 stimulates breast cancer cell growth through ER. This may infer the function of ER in occurrence and development of breast cancer. Together, our study would pave ways for discussing ER concordant TFs and studying other ER-recruited TFs.
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