Suppression of actinomycin D-induced apoptosis by the NS3 protein of hepatitis C virus.

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.