AIM To study the effect of hepatitis C virus nonstructuralprotein 3 c-terminal deleted protein(HCV NS3-5’)onhepatocyte transformation and tumor development.METHODS:QSG7701 cells were transfected with plasmidpRcHCNS3-5’(expressing HCV NS3 c-terminal deletedprotein)by lipofectamine and selected in G418.Theexpression of HCV NS3 gene and protein was determinedby PCR and immunohistochemistry respectively.Biologicalbehavior of transfected cells was observed through cellproliferation assay,anchorage-independent growth andtumor development in nude mice.The expression of HCVNS3 and c-mycproteins in the induced tumor was evaluatedby immunohistochemistry.RESULTS:HCV NS3 was strongly expressed in QSG7701cells transfected with plasmid pRcHCNS3-5’and the positivesignal was located in cytoplasm.Cell proliferation assay showedthat the population doubling time in pRcHCNS3-5’transfectedcells was much shorter than that in pRcCMV and non-transfected cells(24 h,26 h,28 h respectively).The cloningratio of cells transfected with pRcHCNS3-5“ pRcCMV and non-transfected cells was 33 %,1.46 %,1.11%,respectively,the former one was higher than that in the rest two groups(P<0.01).Tumor development was seen in nude miceinoculated with pRcHCNS3-5’transfected cells after 15 days.HE staining showed its feature of hepatocarcinoma,andimmunohistochemistry confirmed the expressions of HCV NS3and c-mycproteins in tumor tissue.The positive control groupinoculated with HepG2 also showed tumor development,whileno tumor developed in the nude mice injected with pRcCMVand non-transfected cells after 40 days.CONCLUSION:1.HCV NS3 c-terminal deleted protein hastransforming and oncogenic potential.2.Human liver cellline QSG7701 may be used as a good model to study HCVNS3 pathogenesis. AIM To study the effect of hepatitis C virus nonstructural protein 3 c-terminal deleted protein (HCV NS3-5 ’) onhepatocyte transformation and tumor development. METHODS: QSG7701 cells were transfected with plasmid pRcHCNS3-5’ expressing HCV NS3 c-terminal deleted protein lipofectamine and selected in G418. Theexpression of HCV NS3 gene and protein was determined by PCR and immunohistochemistry respectively. Biological behavior of transfected cells was observed through cellproliferation assay, anchorage-independent growth and tumor development in nude mice. The expression of HCV NS3 and c-mycoproteins in the induced tumor was evaluated by immunohistochemistry .RESULTS: HCV NS3 was strongly expressed in QSG7701 cells transfected with plasmid pRcHCNS3-5’and the positive signal was located in cytoplasm. Cell proliferation assay showed the population doubling time in pRcHCNS3-5’transfected cells was much shorter than that in pRcCMV and non-transfected cells (24 h, 26 h, 28 h respectively). The cloning scale of c ells transfected with pRcHCNS3-5 ”pRcCMV and non-transfected cells was 33%, 1.46%, 1.11%, respectively, the former one was higher than that in the rest two groups (P <0.01). Tumor development was seen in nude miceinoculated with pRcHCNS3-5’transfected cells after 15 days. HE staining showed its feature of hepatocarcinoma, and immunohistochemistry confirmed the expressions of HCV NS3 and c-mycoproteins in tumor tissue. the positive control group inoculated with HepG2 also showed tumor development, whileno tumor developed in the nude mice injected with pRcCMVand non-transfected cells after 40 days. CONCLUSION: 1. HCV NS3 c-terminal deleted protein hastransforming and oncogenic potential. 2. Human liver cell line QSG7701 may be used as a good model to study HCV NS3 pathogenesis.