Objective： To study the effect of ciglitazone on hepatic cancer cells HepG2 growth in vitro and in vivo and its mechanisms. Methods： The in vitro cultured HepG2 lines were treated with various concentrations of ciglitazone. The in vitro growth of HepG2 cells was examined by growth curve and the cell cycle was analyzed by flow cytometry. HepG2 cells （1×10^6 /mouse） were inoculated subcutaneously into 20 nude mice to establish the hepatocellular carcinoma model. The mice were randomly divided into two groups： the control group （group A, n=10） and the ciglitazone-treated group （group B, n=10）. The mice in the group B were injected with 100μL （100μmol/L） of ciglitazone every other day for 15 times, while the mice in the group A with saline instead. One month later, the weights of the resected subcutaneous tumors and suppression rates were measured. The expression of cyclinD1 and P21 was detected by Western blot. Results： The proliferation of HepG2 was significantly inhibited by ciglitazone in a dose- and timedependant manner. There were more cells arrested in G1/G0 phase and the expression of PPARγ was markedly up-regulated in HepG2 cells treated with ciglitazone. After the treatment with ciglitazone, the average weights of the tumors in the group A and B were 3.73±0.22 g and 2.60±0.35 g, respectively, and the tumor suppression rate in the group B was 30%. The expression of cyclinD1 was increased significantly, while that of P21 was decreased significantly in group A as compared with that in group B. Conclusion： Ciglitazone could significantly inhibit HepG2 proliferation in a dose- and time-dependent manner, and induce differentiation of HepG2, the mechanism of which may be related to the PPARγ intervention to cell cycle control.
