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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >The nucleotide binding motif of hepatitis C virus NS4B can mediate cellular transformation and tumor formation without ha-ras co-transfection
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The nucleotide binding motif of hepatitis C virus NS4B can mediate cellular transformation and tumor formation without ha-ras co-transfection

机译：丙型肝炎病毒NS4B的核苷酸结合基序可以介导细胞转化和肿瘤形成，而无需进行ha-ras共转染

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摘要

Hepatitis C virus (HCV) is an important cause of chronic liver disease and is complicated by hepatocellular carcinoma (HCC). Mechanisms whereby the virus promotes cellular transformation are poorly understood. We hypothesized that the guanosine triphosphatase activity encoded in the HCV NS4B protein's nucleotide binding motif (NBM) might play a role in the transformation process. Here we report that NS4B can transform NIH-3T3 cells, leading to tumor formation in vivo. This transformation was independent of co-transfection with activated Ha-ras. Detailed analyses of NS4B mutants revealed that this transforming activity could be progressively inhibited and completely abrogated by increasing genetic impairment of the NS4B nucleotide binding motif. Conclusion: NS4B has in vitro and in vivo tumorigenic potential, and the NS4B transforming activity is indeed mediated by its NBM. Moreover, our results suggest that pharmacological inhibition of the latter might inhibit not only HCV replication but also the associated HCC.
机译：丙型肝炎病毒（HCV）是慢性肝病的重要原因，并伴有肝细胞癌（HCC）。病毒促进细胞转化的机制了解甚少。我们假设HCV NS4B蛋白的核苷酸结合基序（NBM）中编码的鸟苷三磷酸酶活性可能在转化过程中起作用。在这里，我们报道NS4B可以转化NIH-3T3细胞，从而导致体内肿瘤形成。该转化独立于与活化的Ha-ras的共转染。对NS4B突变体的详细分析表明，通过增加NS4B核苷酸结合基序的遗传损伤，可以逐渐抑制这种转化活性并完全废除该转化活性。结论：NS4B具有体内外致瘤的潜能，NS4B的转化活性确实是由其NBM介导的。此外，我们的结果表明，后者的药理学抑制作用可能不仅抑制HCV复制，而且抑制相关的HCC。

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