Differential ChIP-Seq Analysis of O-GlcNAc and Adriamycin bound Chromatin Loci in Human Breast Cancer Cells

GlcNAcylation is a dynamic post-translational modification that is involved in human diseases and a wide range of biological processes. There is evidence that GlcNAcylation modifies some tumor-associated proteins, but in tumor progression, the role of GlcNAcylation remains unclear. The decrease in cell surface E-cadherin is the molecular mechanism underlying GlcNAcylation-induced breast cancer metastasis. p120 and β-catenin, but not E-cadherin, are GlcNAcylated; the GlcNAcylation of p120 and β- catenin might play roles in the decrease of cell surface E-cadherin. Moreover, immunohistochemistry analysis indicated that the global GlcNAcylation level in breast tumor tissues is elevated significantly as compared to corresponding adjacent tissues; further, GlcNAcylation was significantly enhanced in metastatic lymph nodes compared to their corresponding primary tumor tissues. This study shows that GlcNAcylation enhances the migration/invasion of tumor cells through the analysis of O-GlcNAc protein-bound chromatin loci in human breast cancer cells. This is an important step towards understanding the role of this protein in inducing breast cancer. The main aim of this study is to examine the O-GlcNAc protein-bound chromatin loci in the human breast cancer cells MCF-7 and MCF-7/ADR through differential ChIP-Seq analysis. Also, the prediction and identification of overall binding sites of MCF-7 and MCF-7/ADR cells were performed by the ChIP-seq strategy.