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Cancers 2010, 2(3), 1689-1704; doi:10.3390/cancers2031689

DLEC1 Expression Is Modulated by Epigenetic Modifications in Hepatocelluar Carcinoma Cells: Role of HBx Genotypes

School of Chemical and Biomedical Engineering, Nanyang Technological University, Singapore
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Received: 29 July 2010 / Revised: 23 August 2010 / Accepted: 8 September 2010 / Published: 16 September 2010
(This article belongs to the Special Issue Epigenetics of Cancer Progression)
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Abstract

Deleted in Lung and Esophageal Cancer 1 (DLEC1) is a functional tumor suppressor gene (TSG). It has been found to be silenced in a variety of human cancers including hepatocellular carcinoma (HCC). The silencing of DLEC1 can be modulated by epigenetic modifications, such as DNA hypermethylation and histone hypoacetylation. In the case of HCC, hepatitis B virus X protein (HBx) has been implicated in methylation of target promoters resulting in the down-regulation of tumor suppressor genes, which in turn contributes to the development of HCC. In the present study, we first established a cell system in which epigenetic modifications can be modulated using inhibitors of either DNA methylation or histone deacetylation. The cell system was used to reveal that the expression of DLEC1 was upregulated by HBx in a genotype-dependent manner. In particular, HBx genotype A was found to decrease DNA methylation of the DLEC1 promoter. Our results have provided new insights on the impact of HBx in HCC development by epigenetic modifications.
Keywords: DLEC1; HBV; HBx; DNA methylation; histone acetylation DLEC1; HBV; HBx; DNA methylation; histone acetylation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Niu, D.; Feng, H.; Chen, W.N. DLEC1 Expression Is Modulated by Epigenetic Modifications in Hepatocelluar Carcinoma Cells: Role of HBx Genotypes. Cancers 2010, 2, 1689-1704.

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