Send to

Choose Destination
Exp Ther Med. 2010 May;1(3):519-523. Epub 2010 May 1.

Epigenetic activation of E-cadherin is a candidate therapeutic target in human hepatocellular carcinoma.

Author information

Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education;


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.

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center