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AIM: To examine the expression of human telomerase reverse transcriptase (hTERT) gene in human hepatocellular cancer (HCC), to investigate its relevance with the carcinogenesis, development and recurrence of HCC, and to explore the potential of antisense RNA of human telemerase (hTR) gene in the treatment of HCC. METHODS: Immunohistochemistry was used to detect the expression of hTERT protein in 42 specimens of HCC. The relationship between hTERT expression and the clinical and pathological characteristics was analyzed. HepG2 cell line was transfected with antisense hTR expression vector (pBBS-hTR) with lipofectin. The transfected cells were cultured in vitro and then inoculated into nude mice. The cell cycle, ultrastructure and tumorigenicity of the transfected cells were examined. RESULTS: The positive rate of hTERT gene expression in HCC was significantly higher (30/42) than that in normal liver tissues (71.4% vs 0%, P <0.01), and the positive rates were also significantly different between HCC with pathological grades I (4/10), II(14/20) and III(12/12) (40.0% vs 70.0% vs 100%, respectively, P <0.05). The expression of hTERT was positively correlated to the recurrence of patients (P <0.05). The transfected cells manifested typical apoptotic morphology, and the apoptotic peak appeared before G1 phase of cell cycle. Tumorigenesis of the transfected cells in nude mice was significantly inhibited. The survival time of nude mice inoculated with transfected cells was markedly prolonged, in comparison with that of control mice. CONCLUSION: The aberrant expression of hTERT gene may be related to the pathogenesis and progression of HCC. The highly expressed hTERT gene may be regarded as a marker for the recurrence of HCC. The growth of HepG2 cells can be effectively inhibited and the apoptosis can be promoted by transfection of antisense telomerase RNA.

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Expression of human telomerase reverse transcriptase gene in hepatocellular carcinoma and effect of antisense telomerase gene on apoptosis of hepatocellular cancer cell line HepG2