| Objective:To investigate the effect of connective tissue growth factor(CTGF/CCN2)and peroxisome proliferatoractivated-receptor-γ(PPAR-γ)on the human hepatocellular carcinoma cell,and explore the correlation between the two factors.Methods:(1)Detect the expression of CTGF and PPAR-γprotein in HepG-2 cell and hepatocellular carcinoma by immunohistochemistry.Analyze the correlation between differentiation of hepatocellular carcinoma and expression of the two factors.(2)HepG-2 cell were treated with the ligand of PPAR-γrosiglitazone and antibody of CTGF,at different concentrations for different periods.The proliferation of HepG-2 cell was assessed by MTT.The change of invasion and immigration of HepG-2 cell were detected by boyden.(3)RT-PCR was applied to investigate the expression change of CTGFmRNA which were treated with rosiglitazoneResults:(1)HepG-2 cell and hepatocellular carcinoma expressd CTGF and PPAR-γprotein. immunohistochemistry analysis showed that the protein of CTGF was mainly localized in the cytoplasm.The localization of PPAR-γproteins was in the nucleus and the cytoplasm.(2)Expression of CTGF and differentiation of hepatocellular carcinoma were positive correlation(P＜0.05).But there had no correlation between expression of PPAR-γand differentiation of hepatocellular carcinoma(P＞0.05). (3)The proliferation of HepG-2 cell was inhibited in a time-and dose-dependent manner by using rosiglitazone.The inhibition rate of 20μmoL/L--80μmoL/L groups had a significant difference comparing with the control group(P＜0.05;P＜0.01).No statistic difference of inhibition rate was found between 5μmoL/L 10μmoL/L groups and control groups(P＞0.05).(4)After treated with rosiglitazone,the cell number of invasion and immigration were decreasted,and there had a significant difference comparing with the control group(P＜0.05).(5)The proliferation of HepG-2 cell was inhibited by using anti-CTGF(antibody against CTGF).The inhibition rate of 10μg/mL 20μg/mL 50μg/mL groups had a significant difference comparing with the control group(P＜0.05;P＜0.01).No statistic difference of inhibition rate was found between 5μg/mL groups and control groups(P＞0.05).(6)After treated with anti-CTGF,the cell number of invasion and immigration were decreasted,and there had a significent difference comparing with the control group(P＜0.05).(7)RT-PCR demonstrated that the expression of CTGFmRNA in PPAR-γ-treated cells was down-regulated compared with the control group.Conclusion:(1)HepG-2 cell have the expression of CTGF and PPAR-γprotein.(2)Hepatocellular carcinoma have the expression of CTGF and PPAR-γprotein.Expression of CTGF and differentiation of hepatocellular carcinoma are positive correlation.But there have no correlation between expression of PPAR-γand differentiation of hepatocellular carcinoma.It suggest that the different grade of hepatocellular carcinoma differentiation are closed correlated with CTGF.(3)After treated with rosiglitazone,the proliferation invasion and immigration of HepG-2 cell are inhibited.It suggest that PPAR-γis a important factor which can regulate the biological behaviour of hepatocellular carcinoma.(4)The proliferation invasion and immigration of HepG-2 cell are inhibited when treated with antibody of CTGF.It suggest that CTGF can regulate the development of hepatocellular carcinoma by changing the proliferation invasion and immigration of it.(5)HepG-2 cell have the expression of CTGFmRNA.And the level of CTGFmRNA are blocked by treated with rosiglitazone.It suggest that the mechanism of PPARγregulates the growth of hepatocellular carcinoma cell may be associated with regulating the expression of CTGF.
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