RNA-seq data from MCF-7 cells (breast cancer model) treated with soy extracts
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE56066 | GEO | 2014/10/24
SECONDARY ACCESSION(S): PRJNA242333
REPOSITORIES: GEO
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2008-04-10 | E-GEOD-9936 | biostudies-arrayexpress
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Project description:To understand the complex mechanism of estrogen action, multiple assays based on different biological principles is important. Here, multiple assays based on cell, protein and transcription assays were used to evaluate estrogenic activity of soymilk extracts before and after fermentation, and four soy compounds, genistein and daidzein, and their glycosides, genistin and daidzin, respectively. The data obtained by a transcription assay, RNA-sequencing (RNA-seq), was further examined by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) database analysis to understand cell functions, i.e. biological processes and metabolic pathways. Among the cell functions identified, the sets of genes for cell division/cell cycle and DNA replication/DNA repair are significantly up-regulated, whereas those for autophagy are significantly down-regulated, which explains well the enhanced activity of cell proliferation by these materials. The applications of estrogenic activity of soymilk extracts and soy flavonoids, and the contribution of fermentation, include pharmacological benefits, such as bone protection/bone regeneration, cancer chemoprevention, neuroprotection and the treatment of menopausal syndromes.
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Project description:The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using ChIP-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2-HA protein. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 3 treatments (Veh, Dox, DoxTam) were performed in duplicates. After treatments, cells were collected for ChIP experiment with HA antibody. ChIP-seq libraries were sequenced and data analysis showed almost no binding in Veh treatment, indicating low backgroud and good quality of the data. PAX transcription factor motif were enriched in PAX2 peaks, indicating the reliability of the data. When crossing the ChIP-seq data with genes regulated by PAX2 in MCF-7, we could observe high level binding of PAX2 to prmoters of PAX2 up-regulated genes and the center of intergenic transcripts induced by PAX2, suggesting the role of PAX2 in regulating transcription activation.
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