Human cytidine deaminases facilitate hepatitis B virus evolution and link inflammation and hepatocellular carcinoma

被引：71
作者：
Deng, Yang [1 ]
Du, Yan [1 ]
Zhang, Qi [1 ]
Han, Xue [2 ]
Cao, Guangwen [1 ]
机构：
[1] Second Mil Med Univ, Dept Epidemiol, Shanghai 200433, Peoples R China
[2] Ctr Dis Control & Prevent Yangpu Dist, Div Chron Dis, Shanghai, Peoples R China
来源：
CANCER LETTERS | 2014年 / 343卷 / 02期
关键词：
Cytidine deaminase; Chronic HBV infection; HBV mutation; Hepatocellular carcinoma; Somatic mutation; Evolution; NF-KAPPA-B; HUMAN-IMMUNODEFICIENCY-VIRUS; ASYMPTOMATIC CARRIER STATE; RNA EDITING ENZYME; CORE PROMOTER; X PROTEIN; E-ANTIGEN; HUMAN HEPATOCYTES; SOMATIC HYPERMUTATION; ANTIVIRAL TREATMENT;
D O I：
10.1016/j.canlet.2013.09.041
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
During hepatitis B virus (HBV)-induced hepatocarcinogenesis, chronic inflammation facilitates the evolution of hepatocellular carcinoma (HCC)-promoting HBV mutants. Cytidine deaminases, whose expression is stimulated by inflammatory cytokines and/or chemokines. play an important role in bridging inflammation and HCC. Through G-to-A hypermutation, cytidine deaminases inhibit HBV replication and facilitate the generation of HCC-promoting HBV mutants including C-terminal-truncated HBx. Cytidine deaminases also promote cancer-related somatic mutations including TP53 mutations. Their editing efficiency is counteracted by uracil-DNA glycosylase. Understanding the effects of cytidine deaminases in HBV-induced hepatocarcinogenesis and HCC progression will aid in developing efficient prophylactic and therapeutic strategies against HCC in HBV-infected population. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：161 / 171
页数：11
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