Zeisel Mirjam B, Guerrieri Francesca, Levrero Massimo
Cancer Research Center of Lyon (CRCL), UMR Inserm 1052 CNRS 5286 Mixte CLB, Université de Lyon 1 (UCBL1), 69003 Lyon, France.
Hospices Civils de Lyon, Hôpital Croix Rousse, Service d'Hépato-Gastroentérologie, 69004 Lyon, France.
J Clin Med. 2021 Apr 16;10(8):1715. doi: 10.3390/jcm10081715.
Hepatocellular carcinoma (HCC) is the most frequent primary malignancy of the liver and a leading cause of cancer-related deaths worldwide. Although much progress has been made in HCC drug development in recent years, treatment options remain limited. The major cause of HCC is chronic hepatitis B virus (HBV) infection. Despite the existence of a vaccine, more than 250 million individuals are chronically infected by HBV. Current antiviral therapies can repress viral replication but to date there is no cure for chronic hepatitis B. Of note, inhibition of viral replication reduces but does not eliminate the risk of HCC development. HBV contributes to liver carcinogenesis by direct and indirect effects. This review summarizes the current knowledge of HBV-induced host epigenetic alterations and their association with HCC, with an emphasis on the interactions between HBV proteins and the host cell epigenetic machinery leading to modulation of gene expression.
肝细胞癌（HCC）是最常见的肝脏原发性恶性肿瘤，也是全球癌症相关死亡的主要原因。尽管近年来HCC药物研发取得了很大进展，但治疗选择仍然有限。HCC的主要病因是慢性乙型肝炎病毒（HBV）感染。尽管有疫苗，但仍有超过2.5亿人慢性感染HBV。目前的抗病毒疗法可以抑制病毒复制，但迄今为止慢性乙型肝炎仍无法治愈。值得注意的是，抑制病毒复制可降低但不能消除HCC发生的风险。HBV通过直接和间接作用促进肝癌发生。本综述总结了目前关于HBV诱导的宿主表观遗传改变及其与HCC关联的知识，重点关注HBV蛋白与宿主细胞表观遗传机制之间导致基因表达调控的相互作用。
