Objective: To explore the effects and mechanisms of hepatocyte growth factor (HGF)/C-Met transduction system on the growth, invasion and transmission of hepatocellular carcinoma.Methods: Hepatocarcinoma HepSB cell line was divided into five groups. In the groupj A ( control group ) HGF was not used. In the groupi B, C, D and E, HGF was used with different concentrations. Acorrding to the grouping of hepatocellular Hep3B cell line, normal hepatocytes were also divided into five groups. In the group2 (control group) HGF was not used. In the group2 2,3,4 and 5, HGF was used with different concentrations. After treated with HGF on different doses, the cell proliferation and scatter of hepatocarcinoma HepSB cells and normal hepatocytes were examined to compare the results with each group. Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect the Vascular Endothelial Growth Factor (VEGF) concentration in the culture supernatant of hepatocarcinoma Hep3B cells. Immunohistochemistry technique was used to exam the Proliferating Cell Nuclear Antigen (PCNA) in hepatocarcinoma HepSB cells with Proliferating Cell Nuclear Antigen Label Index (PCNA-LI).Results: (1) The proliferation and scatter degree of hepatocarcinoma HepSB cell were significantly increased after treated with HGF in the concentrations of 1~15ng.ml-1,which presented a dose-dependent manner and cells modality alteration. When the concentration of HGF was 20ng.mr1, the cell proliferation stopped to apoptosis, while the proliferation of normal hepatocytes went on. (2) The Optical Density (OD) value of VEGF protein was significantly higher in the groups of B, C and D compared with the control one. In the groups of B, C and D, the PCNA-LI was significantly higher than that in the control. However, there is no difference between group E and the control with VEGF and PCNA-LI results.Conclusions: Our study proved that HGF/c-met signal transduction system could promote the proliferation, invasion and metastasis of hepatocyte, which was affected by the concentration of HGF. The mechanism is probably related to the proliferation, scatter, high expression of VEGF and PCNA.
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