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

by 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
Cancers 2016, 8(8), 76; https://doi.org/10.3390/cancers8080076
Received: 20 June 2016 / Revised: 1 August 2016 / Accepted: 15 August 2016 / Published: 20 August 2016
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
MDPI and ACS Style

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

AMA Style

Tian Y, Mok MTS, Yang P, Cheng ASL. Epigenetic Activation of Wnt/β-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis. Cancers. 2016; 8(8):76.

Chicago/Turabian Style

Tian, Yuan; Mok, Myth T.S.; Yang, Pengyuan; Cheng, Alfred S.L. 2016. "Epigenetic Activation of Wnt/β-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis" Cancers 8, no. 8: 76.

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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