title: Epigenetic activation of E-cadherin is a candidate therapeutic target in human hepatocellular carcinoma.
abstract: E-cadherin is a key cell adhesion molecule implicated in tumor suppression that is frequently altered in hepatocellular carcinoma (HCC), particularly in hepatitis B virus-related tumors. Here, we report that the epigenetic drugs 5-azacytidine and trichostatin A up-regulated E-cadherin expression in HCC cells. The depletion of DNMT1 restored E-cadherin expression via demethylation, whereas the depletion of DNMT3A or DNMT3B did not. Activated E-cadherin suppressed HCC cell colony formation. However, E-cadherin expression was repressed by HBx transfection due to the DNA methylation induced by the elevation of DNMT1 in the HCC cell lines. The present study indicates that E-cadherin expression is regulated by epigenetic agents in HCC cells, which suggests a schema for restoring E-cadherin by targeting its epigenetic mechanism.
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education;
authors.forename: Xuemei
authors.initials: X
authors.lastname: Qiu
authors.forename: Fengchang
authors.initials: F
authors.lastname: Qiao
authors.forename: Xianwei
authors.initials: X
authors.lastname: Su
authors.forename: Zhujiang
authors.initials: Z
authors.lastname: Zhao
authors.forename: Hong
authors.initials: H
authors.lastname: Fan