The smallest protein of hepatitis B virus (HBV), HBx, has been implicated in the development of liver diseases by interfering with normal cellular progresses. Its role in cell proliferation has been unclear as both pro-apoptotic and anti-apoptotic activities have been reported. We showed molecular evidence that HBx induced apoptosis in HepG2 cells. ABcl-2 Homology Domain 3 (BH3) was identified in HBx, which interacted with anti-apoptotic but not pro-apoptotic members of the Bcl-2 family of proteins. HBx induced apoptosis when transfected into HepG2 cells, as demonstrated by both flow cytometry and caspase-3 activity. However, HBx protein may not be stable in apoptotic cells triggered by its own expression as only its mRNA or the fusion protein with the glutathione-S-transferase was detected in transfected cells. These results suggested that HBx behaved as a pro-apoptotic protein and was able to induce apoptosis.

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