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.

journal_name

Exp Ther Med

authors

Qiu X,Qiao F,Su X,Zhao Z,Fan H

doi

10.3892/etm_00000082

subject

Has Abstract

pub_date

2010-05-01 00:00:00

pages

519-523

issue

3

eissn

1792-0981

issn

1792-1015

pii

etm-01-03-0519

journal_volume

1

pub_type

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