Feitelson M A
Room 222 Alumni Hall, Department of Pathology, Anatomy and Cell Biology and Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107-6799, USA.
J Hepatobiliary Pancreat Surg. 1998;5(4):367-74. doi: 10.1007/s005340050060.
Hepatitis B virus (HBV) is one of the major etiological agents responsible for the appearance of chronic liver diseases, including hepatocellular carcinoma (HCC). There is increasing evidence that the HBV excoded x antigen (HBxAg) is involved in one or more steps that contribute to multistep hepatocarcinogenesis. Recent work has now defined one of these steps as the physical binding and functional inactivation of the tumor suppressor protein, p53, by HBxAg. The centrality of p53 to genomic stability, cell cycle arrest, induction of apoptosis, and in senescence related pathways, suggests that its disruption by HBxAg will result in genomic instability, loss of cell cycle control, a lower apoptotic rate, and an extension in the life span of HBV-infected cells. It is proposed that HBxAg/p53 complex formation represents one of several steps whereby HBV contributes to the development of HCC.
乙型肝炎病毒（HBV）是导致包括肝细胞癌（HCC）在内的慢性肝病出现的主要病原体之一。越来越多的证据表明，HBV编码的X抗原（HBxAg）参与了导致多步骤肝癌发生的一个或多个步骤。最近的研究现已将其中一个步骤定义为HBxAg对肿瘤抑制蛋白p53的物理结合和功能失活。p53在基因组稳定性、细胞周期停滞、细胞凋亡诱导以及衰老相关途径中的核心地位表明，HBxAg对其的破坏将导致基因组不稳定、细胞周期控制丧失、凋亡率降低以及HBV感染细胞寿命延长。有人提出，HBxAg/p53复合物的形成是HBV促成HCC发生的几个步骤之一。
