Chromatin immunoprecipitation-sequencing predicts p300 binding sites in the MCF7 human breast cancer cell line.

The aim of the present study was to identify the distribution characters of p300 binding sites in estradiol (E2) stimulated MCF7 cell lines and controls, and to study the roles of transcriptional coactivator p300 in the tumorigenesis and progression of various human cancers following E2 stimulation. The chromatin immunoprecipitation followed by sequencing data of GSES9623 was downloaded from the Gene Expression Omnibus database, including breast cancer data of GSM986085 and control data of GSM986087. MACS peak‑calling software was employed to identify the p300‑bound sites in the two groups. The differential target genes of p300‑bound sites were further analyzed and the concordant factors were predicted. The Gene Ontology (GO) was used to conduct functional enrichment analysis. There were 32,249 p300 binding sites identified in the E2 stimulation group and 43,156 in the control group. GO enrichment analysis of the target genes showed that p300‑regulated target genes mainly participated in the neural cell differentiation‑associated biology process; while in the E2 stimulation group, partial functions of the target genes had changed. A total of 24,899 differential p300‑bound sites of the two groups were identified and GO enrichment analysis demonstrated that E2 stimulation changed p300 binding sites, but did not influence the regulatory function of p300. The effect of E2 in the MCF7 cells suggested that E2 affected the binding affinity of DNA and transcription factors in a large scale. By analyzing the concordant factors, several important factors were discovered, such as BRCA1 and ESR1. Overall, the results of the present study suggested an association between p300 and carcinogenic genes. This may provide theoretical guidance for cancer therapy.