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AIM:To investigate the effects of p16 gene on biologicabehavious in hepatocellular carcinoma cells.METHODS:HCC cell lines SNU-449 and HepG2.2.15 wereinfected respectively by a replication defective,recombinantretrovirus capable of producing a high level of p16 proteinexpression(pCLXSN-p16).G418 resistant stable P16 proteinexpression cell lines were selected.And the biological behavioursof the p16 gene transfected HCC cells were observed.RESULTS:Initial in vitro experiments in HCC cell line SNU-449 with loss of p16 protein expression demonstrated thepCLXSN-p16 treatment significantly inhibited cell growth.But there was no treatment effect when the pCLXSN-p16was used in another HCC cell line HepG2.2.15 which haspositive p16 protein expression.Subsequent study in a nudemouse model demonstrated that the p16 gene transfectedSNU-449 had a lower succeeding rate in the first timeestablishment of tumors and grew more slowly in the nudemice when compared with non-transfected SNU-449.Moreover,the nude mice inoculated with transfected SNU-449 had a longer surviving time than those inoculated withnon-transfected SNU-449.CONCLUSION:Our results show that the p16INK4a genetransfer can inhibit the proliferation and reduce the invasionability of hepatocellular carcinoma.
AIM: To investigate the effects of p16 gene on biologic abbey in hepatocellular carcinoma cells. METHODS: HCC cell lines SNU-449 and HepG2.2.15 were infected respectively by a replication defective, recombinant retrovirus capable of producing a high level of p16 proteinexpression (pCLXSN- p16) .G418 resistant stable P16 proteinexpression cell lines were selected. And the the biological behaviors of the p16 gene transfected HCC cells were observed .RESULTS: Initial in vitro experiments in HCC cell line SNU-449 with loss of p16 protein expression rendered the pCLXSN-p16 cell growth. There was no treatment effect when the pCLXSN-p16 was used in another HCC cell line HepG2.2.15 which has positive p16 protein expression. Subsequent study in a nudemouse model of the p16 gene transfected SU-449 had a lower succeeding rate in the first timeestablishment of tumors and grew more slowly in the nudemice when compared with non-transfected SNU-449. Moreover, the nude mice inoculated with transfected SNU-449 had a longer surviving time than those inoculated with non-transfected SNU-449. CONCLUSION: Our results show that the p16INK4a genetransfer can inhibit the proliferation and reduce the invasionability of hepatocellular carcinoma.