Ding SL, Yang ZW, Wang J, Zhang XL, Chen XM, Lu FM. Integrative analysis of aberrant Wnt signaling in hepatitis B virus-related hepatocellular carcinoma. World J Gastroenterol 2015; 21(20): 6317-6328 [PMID: 26034368 DOI: 10.3748/wjg.v21.i20.6317]
Corresponding Author of This Article
Feng-Min Lu, PhD, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China. lu.fengmin@bjmu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Systematic Reviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. May 28, 2015; 21(20): 6317-6328 Published online May 28, 2015. doi: 10.3748/wjg.v21.i20.6317
Integrative analysis of aberrant Wnt signaling in hepatitis B virus-related hepatocellular carcinoma
Shan-Long Ding, Zi-Wei Yang, Jie Wang, Xiao-Lei Zhang, Xiang-Mei Chen, Feng-Min Lu
Shan-Long Ding, Zi-Wei Yang, Jie Wang, Xiao-Lei Zhang, Xiang-Mei Chen, Feng-Min Lu, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China
Author contributions: Wang J, Chen XM, and Lu FM designed the study; Ding SL, Yang ZW, and Zhang XL performed the majority of the experiments; Ding SL wrote the manuscript; and Lu FM edited the manuscript.
Supported by National Natural Science Foundation of China, No. 81372603; 973 Program, No. 2015CB554000; National S T Major Project for Infectious Diseases, No. 2012ZX10004-904; and The 111 Project, No. B07001.
Conflict-of-interest: The authors declare no conflicts of interest related to this manuscript.
Data sharing: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Feng-Min Lu, PhD, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China. lu.fengmin@bjmu.edu.cn
Telephone: +86-10-82805136 Fax: +86-10-82805136
Received: December 21, 2014 Peer-review started: December 22, 2014 First decision: January 8, 2015 Revised: January 22, 2015 Accepted: March 12, 2015 Article in press: March 12, 2015 Published online: May 28, 2015 Processing time: 159 Days and 20 Hours
Core Tip
Core tip: Abnormal activation of Wnt/β-catenin signaling can be detected in approximately 50%-70% of hepatocellular carcinoma (HCC). It is necessary to take the analysis about the cause of Wnt/β-catenin signaling pathway aberration with the etiologic differences into consideration. In this review, the suggested genetic/epigenetic aberrations and their involvement in the abnormal Wnt/β-catenin overactivation in HCC were comprehensively analyzed, with focus on the cause of hepatitis B virus-related HCC. We suggest that genetic/epigenetic aberration of CTNNB1 and its protein degradation regulators are the major cause of Wnt signaling overactivation. TP53 gain-of-function mutation is seldom involved, and HBx-LINE1 chimeric transcripts created by viral integration may not be present.
