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乙肝X抗原刺激一种新型细胞基因URG4的表达，该基因可促进肝细胞的生长和存活。

Hepatitis Bx antigen stimulates expression of a novel cellular gene, URG4, that promotes hepatocellular growth and survival.

作者信息

Tufan N Lale Satiroglu, Lian Zhaorui, Liu Jie, Pan Jingbo, Arbuthnot Patrick, Kew Michael, Clayton Marcy M, Zhu Minghua, Feitelson Mark A

机构信息

Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107-6799, USA.

出版信息

Neoplasia. 2002 Jul-Aug;4(4):355-68. doi: 10.1038/sj.neo.7900241.

DOI:10.1038/sj.neo.7900241

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1531705/

Abstract

Hepatitis B virus encoded X antigen (HBxAg) may contribute to the development of hepatocellular carcinoma (HCC) by up- or downregulating the expression of cellular genes that promote cell growth and survival. To test this hypothesis, HBxAg-positive and -negative HepG2 cells were constructed, and the patterns of cellular gene expression compared by polymerase chain reaction select cDNA subtraction. The full-length clone of one of these upregulated genes (URG), URG4, encoded a protein of about 104 kDa. URG4 was strongly expressed in hepatitis B-infected liver and in HCC cells, where it costained with HBxAg, and was weakly expressed in uninfected liver, suggesting URG4 was an effector of HBxAg in vivo. Overexpression of URG4 in HepG2 cells promoted hepatocellular growth and survival in tissue culture and in soft agar, and accelerated tumor development in nude mice. Hence, URG4 may be a natural effector of HBxAg that contributes importantly to multistep hepatocarcinogenesis.

摘要

乙型肝炎病毒编码的X抗原（HBxAg）可能通过上调或下调促进细胞生长和存活的细胞基因表达，从而促进肝细胞癌（HCC）的发生发展。为验证这一假说，构建了HBxAg阳性和阴性的HepG2细胞，并通过聚合酶链反应选择cDNA消减技术比较细胞基因表达模式。其中一个上调基因（URG）即URG4的全长克隆编码一种约104 kDa的蛋白质。URG4在乙型肝炎感染的肝脏和HCC细胞中强烈表达，且与HBxAg共染色，而在未感染的肝脏中弱表达，提示URG4是HBxAg在体内的效应分子。URG4在HepG2细胞中的过表达在组织培养和软琼脂中促进了肝细胞生长和存活，并加速了裸鼠肿瘤的发展。因此，URG4可能是HBxAg的天然效应分子，对肝细胞癌的多步骤发生发展起重要作用。