Fujita T, Ishido S, Muramatsu S, Itoh M, Hotta H
Department of Microbiology, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650, Japan.
Biochem Biophys Res Commun. 1996 Dec 24;229(3):825-31. doi: 10.1006/bbrc.1996.1887.
The NS3 protein of hepatitis C virus is a multifunctional protein that is indispensable for virus replication. Little is known, however, about the possible effects of the NS3 on host cell function(s). In the present study, we demonstrated that NIH3T3 cells constitutively expressing a carboxy-terminally truncated NS3 (NS3DeltaC) were more resistant to actinomycin D-induced apoptosis than the control cells. We also observed that induction of p53 expression by actinomycin D treatment was weaker in the NS3DeltaC-expressing cells than in the control cells. However, induction of WAF1 expression by the same treatment was not different between the two groups. Taken together, our results suggest the possibility that expression of NS3DeltaC suppressed actinomycin D-induced apoptosis of NIH3T3 cells through at least partly, if not solely, a p53-dependent, WAF1-independent pathway.
丙型肝炎病毒的NS3蛋白是一种多功能蛋白，对病毒复制不可或缺。然而，关于NS3对宿主细胞功能可能产生的影响，人们知之甚少。在本研究中，我们证明，组成性表达羧基末端截短型NS3（NS3DeltaC）的NIH3T3细胞比对照细胞对放线菌素D诱导的凋亡更具抗性。我们还观察到，放线菌素D处理诱导的p53表达在表达NS3DeltaC的细胞中比在对照细胞中更弱。然而，两组之间相同处理诱导的WAF1表达没有差异。综上所述，我们的结果表明，NS3DeltaC的表达至少部分地（如果不是完全地）通过p53依赖、WAF1非依赖的途径抑制了放线菌素D诱导的NIH3T3细胞凋亡。
