Linlin Ma , Shuzhen Chen , Hongyang Wang , Lei Chen
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引用次数: 0
摘要
乙型肝炎病毒（HBV）是导致肝细胞癌（HCC）的最常见原因，HCC是东南亚主要的肝癌类型。全世界约有3.5亿人患有持续性乙型肝炎感染。HBV通过直接和间接机制促进HCC的发展。在肿瘤发生的初始阶段，HBV DNA整合到宿主基因组中，导致癌症相关基因的插入突变和基因组不稳定。形成染色体外环状DNA (ecDNA)，其被大量高效扩增以表达病毒基因和宿主癌基因。此外，病毒相关蛋白，如HBV X （HBx）调节蛋白和/或修饰的preS/S包膜蛋白，可以改变宿主细胞中与多种功能相关的基因的表达。本文就HBx和preS/S蛋白在促进肿瘤发生中的作用进行综述。总结了hbv相关肿瘤发生的具体机制，并讨论了今后研究的问题和展望。
Hepatitis B virus integration and hepatocarcinogenesis
Hepatitis B virus (HBV) is the most common cause of hepatocellular carcinoma (HCC), which is the predominant liver cancer type in Southeast Asia. Approximately 350 million individuals suffer from persistent hepatitis B infection worldwide. HBV promotes HCC development through direct and indirect mechanisms. HBV DNA integrates into the host genome during the initial stages of tumorigenesis, causing insertional mutagenesis of cancer-related genes and genomic instability. Extrachromosomal circular DNA (ecDNA) is formed, which is efficiently amplified in large quantities to express viral genes and host oncogenes. Moreover, virus-associated proteins, such as the regulatory HBV X (HBx) protein and/or the modified preS/S envelope protein, alter the expression of genes associated with multiple functions in host cells. In this review, we summarize the role of the HBx and preS/S proteins in promoting tumorigenesis. In addition to summarizing the specific mechanism of HBV-related tumorigenesis, the concerns and perspectives for future study are discussed.
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