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Cancers 2016, 8(8), 76; doi:10.3390/cancers8080076

Epigenetic Activation of Wnt/β-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis

1,†
,
2,3,†
,
1,* and 2,3,4,*
1
Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
2
School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
3
Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen 518057, China
4
State Key Laboratory of Digestive Disease and Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Samy L. Habib
Received: 20 June 2016 / Revised: 1 August 2016 / Accepted: 15 August 2016 / Published: 20 August 2016
View Full-Text   |   Download PDF [227 KB, uploaded 20 August 2016]

Abstract

Non-alcoholic fatty liver disease (NAFLD), characterized by fat accumulation in liver, is closely associated with central obesity, over-nutrition and other features of metabolic syndrome, which elevate the risk of developing hepatocellular carcinoma (HCC). The Wnt/β-catenin signaling pathway plays a significant role in the physiology and pathology of liver. Up to half of HCC patients have activation of Wnt/β-catenin signaling. However, the mutation frequencies of CTNNB1 (encoding β-catenin protein) or other antagonists targeting Wnt/β-catenin signaling are low in HCC patients, suggesting that genetic mutations are not the major factor driving abnormal β-catenin activities in HCC. Emerging evidence has demonstrated that obesity-induced metabolic pathways can deregulate chromatin modifiers such as histone deacetylase 8 to trigger undesired global epigenetic changes, thereby modifying gene expression program which contributes to oncogenic signaling. This review focuses on the aberrant epigenetic activation of Wnt/β-catenin in the development of NAFLD-associated HCC. A deeper understanding of the molecular mechanisms underlying such deregulation may shed light on the identification of novel druggable epigenetic targets for the prevention and/or treatment of HCC in obese and diabetic patients. View Full-Text
Keywords: non-alcoholic fatty liver disease; hepatocellular carcinoma; Wnt; β-catenin; epigenetics; DNA methylation; histone modification; microRNA; HDAC8 non-alcoholic fatty liver disease; hepatocellular carcinoma; Wnt; β-catenin; epigenetics; DNA methylation; histone modification; microRNA; HDAC8
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Tian, Y.; Mok, M.T.; Yang, P.; Cheng, A.S. Epigenetic Activation of Wnt/β-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis. Cancers 2016, 8, 76.

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