NF-κB activation by hepatitis B virus X (HBx) protein shifts the cellular fate toward survival

In this paper, we examined the cellular effect of hepatitits B virus X (HBx) in ChangX-34 cells, inducible HBx-expressing cells. High expression of HBx protein in ChangX-34 cells resulted in approximately three-fold increase in DNA synthesis and did not show apoptotic changes. Expression of HBx in these cells was accompanied by the NF-κB-mediated transcription. Interestingly, inhibition of NF-κB activity either by treatment with sulfasalazine, a specific inhibitor of NF-κB, or by expressing IκBα super-repressor significantly increased cell death in ChangX-34 cells but had no influence on parental Chang cells. Thus, the activation of NF-κB in HBx-expressing cells may play a critical role in shifting the balance toward cell survival.