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  • Title: [The influence of HBV infection on TRAIL-induced apoptosis and its mechanism].
    Author: Han L, Sun W, Ma C, Zhang L, Cao Y, Song J, Chen Y.
    Journal: Zhonghua Yi Xue Za Zhi; 2002 May 10; 82(9):597-600. PubMed ID: 12133479.
    Abstract:
    OBJECTIVE: The aim of this study was to investigate whether Hepatitis B virus will influence TRAIL (TNF-related apoptosis inducing ligand) induced apoptosis of the target cells. METHODS: Two human hepatocellular carcinoma cell lines, HepG2 and its HBV whole genome transgenic cell line named HepG2.2.15 were observed in the experiments. The apoptosis rates of these two cell lines to TRAIL were examined by flow cytometry. The expression of the membrane-bound TRAIL and the secretory soluble TRAIL in the supernatant were assessed by flow cytometry and enzyme-linked immunosorbent assay, respectively. The expression of the mRNA of TRAIL receptors and FLIP were assessed by semi-quantitive PCR. RESULTS: In contrast to HepG2 cell line, the apoptosis rate of HepG2.2.15 cell line to TRAIL was significantly low (9.12% vs 51.6%, P < 0.01). The mRNA expression of four TRAIL receptors related to apoptosis were decreased to a more or less degree on HepG2.2.15 cells compared with HepG2 cells, but the expression of FLIP, a protein inhibiting apoptosis at the initial level of the caspase cascade, was drastically upregulated on HepG2.2.15 cells (P < 0.01). There's no significant difference in the secretory TRAIL expression between these two cell lines. CONCLUSION: Our results indicate that HBV could make cells resistant to TRAIL-induced apoptosis, this may be realized by the down-regulated expression of TRAIL and its receptors and up-regulated expression of FLIP. This offer us another explanation why HBV could escape the immune surveillance and persistently exist in the body, which may explain the pathogenesis of HBV related disease in a novel way.
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