Expression of fas ligand in human hepatoma cell lines: Role of hepatitis-Bvirus X (HBx) in induction of Fas ligand

It has been postulated that tumor cells expressing Fas ligand (FasL) can ev ade immune surveillance by inducing apoptosis in T cells expressing Fas. In this study, we investigated Fast expression in 13 human hepatoma cell line s. Strong Fast expression was detected by reverse transcription-polymerase chain reaction or immunofluorescence in Hep G2.2.15, in which the hepatitis -B-virus (HBV) genome was transfected, and in SNU-354, which showed HBx tra nscripts. To determine the biological activity of Fast, Hep G2.2.15 was co- cultured with MOLT-4, T-cell-leukemia cells. Hep G2.2.15 induced apoptosis in MOLT-4 and this was inhibited by the antagonistic anti-Fas antibody, ZB4 . For further analysis of the role of HBx in the induction of Fast, PLC/PRF /5 cells were transfected transiently with the HBV genome, or HBx, or the f rameshift mutant of HBx. In PLC/PRF/5 cells transfected with the HBV genome or HBx but not in cells transfected with the frameshift mutant of HBx, Fas t expression was detected. Our data suggest that HBx plays a role in the in duction of Fast in hepatoma cells and in the escape from immune surveillanc e. (C) 1999 Wiley-Liss, Inc.