AIM:To transfect murine angiostatin cDNA into humanhepatocellular carcinoma cell line SMMC-7721 and toinvestigate its effects on implanted carcinoma in nude mice.METHODS:A eukaryotic expression vector of pcDNA3.1-mAST containing murine angiostatin was constructed.ThenpcDNA3.1-mAST plasmid was transfected into cell line SMMC-7721 by Lipofectamine.The resistant clone was screenedby G418 filtration and identified by RT-PCR and Westernblotting.Nude mice were divided into three groups of 10each.Mice in blank control group were only injected withSMMC-7721 cells.Mice in vector control group were injectedwith SMMC-7721 cells transfected with pcDNA3.1 (+) vector,whereas mice in angiostatin group were injected with SMMC-7721 cells transfected with pcDNA3.1-mAST plasmid.Volume,mass and microvessel density (MVD) of the tumorsin different groups were measured and compared.RESULTS:Murine angiostatin cDNA was successfullycloned into the eukaryotic expression vector pcDNA3.1 (+).pcDNA3.1-mAST was successfully transfected into SMMC-7721 cell line and showed stable expression in this cell line.No significant difference was observed in the growth speedof SMMC-7721 cells between groups transfected with andwithout angiostatin cDNA.Tumor volume,mass and MVD inthe angiostatin group were significantly lower than those inthe blank control group and vector control group (P<0.01).The inhibitory rate of tumor reached 78.6%.Mass and MVDof the tumors only accounted for 34.6% and 48.9% respectivelyof those in the blank control group.CONCLUSION:Angiostatin cDNA could be stably expressedin human hepatocellular carcinoma cell line SMMC-7721without obvious inhibitory effects on the growth of SMMC-7721 cells.When implanted into nude mice,SMMC-7721cells transfected with angiostatin cDNA show a decreasedtumorigenic capability.It suggests that angiostatin caninhibit tumor growth through its inhibition on angiogenesisin tumors. AIM: To transfect murine angiostatin cDNA into human hepatocellular carcinoma cell line SMMC-7721 and to investigate its effects on implanted carcinoma in nude mice. METHODS: A eukaryotic expression vector of pcDNA3.1-mAST containing murine angiostatin was constructed. Chenp cDNA 3.1-mAST plasmid was transfected into cell line SMMC-7721 by Lipofectamine. The resistant clone was screenedby G418 filtration and identified by RT-PCR and Western blotting. Nude mice were divided into three groups of 10 leaves. Micr in blank control group were only injected with SMMC-7721 cells. Mice in vector control group were injected with SMMC-7721 cells transfected with pcDNA3.1 (+) vector, the mice in angiostatin group were injected with SMMC-7721 cells transfected with pcDNA3.1-mAST plasmid. Volume, mass and microvessel density (MVD ) of the tumorsin different groups were measured and compared .RESULTS: Murine angiostatin cDNA was successfullycloned into the eukaryotic expression vector pcDNA3.1 (+). pcDNA3.1-mAST was succ essfully transfected into SMMC-7721 cell line and showed stable expression in this cell line. No significant difference was observed in the growth speed of SMMC-7721 cells between groups transfected with and with angiostatin cDNA. Tumor volume, mass and MVD inthe angiostatin group were significantly lower than those inthe blank control group and vector control group (P <0.01) .The inhibitory rate of the tumor reached 78.6% .Mass and MVD of the tumors only accounted for 34.6% and 48.9% respectivelyof those in the blank control group.CONCLUSION: Angiostatin cDNA could be stably expressed in human hepatocellular carcinoma cell line SMMC-7721without significant inhibitory effects on the growth of SMMC-7721 cells. WHhen implanted into nude mice, SMMC-7721 cells transfected with angiostatin cDNA show a decreased tumorigenic capability. It suggests that angiostatin caninhibit tumor growth through its inhibition on angiogenesis in tumors.