Hepatitis B virus and hepatocellular carcinoma: a possible role for the viral transactivators.
Hepatitis B virus and hepatocellular carcinoma: a possible role for the viral transactivators.
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乙型肝炎病毒和肝细胞癌：病毒反式激活剂的可能作用。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
H. Will
中科院分区：
文献类型：
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作者：
M. Levrero;C. Balsano;M. Avantaggiati;G. Natoli;E. de Marzio;H. Will
一些流行病学研究表明慢性乙型病毒感染与原发性肝细胞癌（PHC）之间存在联系。在肝癌组织中经常观察到HBV DNA序列整合到宿主细胞基因组中。然而，由于仅在少数PHC病例中确定了HBV-DNA插入的靶点，因此对hbv诱导肝细胞转化的其他机制进行了研究。像许多其他DNA病毒一样，乙型肝炎病毒具有交互激活的潜力。HBV X蛋白的全长和截短版本都能够影响细胞核原癌基因c-fos和c-myc的表达。第二种转录激活因子由HBV的PreS/S区编码，但其对病毒和细胞基因的活性只有在其下游序列脱位后才显现出来。因此，HBV能够通过天然蛋白、新生成的截断蛋白和病毒细胞融合多肽影响感染细胞的生长和分化。
Several epidemiological studies have demonstrated a link between chronic B virus infection and primary hepatocellular carcinoma (PHC). HBV DNA sequence integrations into the host cell genome have often been observed in hepatocarcinoma tissues. However, since only in a few cases of PHC the target of HBV-DNA insertion has been identified, alternative mechanisms for HBV-induced hepatocyte transformation have been investigated. Like many other DNA viruses, the hepatitis B virus bears a transactivational potential. Both full length and truncated versions of HBV X protein are able to influence the expression of cellular nuclear protooncogenes c-fos and c-myc. A second transcriptional activator is encoded by the PreS/S region of HBV, but its activity on viral and cellular genes become evident only after dislocations from its downstream sequences. Thus, HBV is able to influence infected cell growth and differentiation using both native proteins, newly generated truncated proteins and virus-cell fusion polypeptides.