Dehydrolovastatin inhibited proliferation and enhanced its chemosensitivity to cisplatin on hepatocellular carcinoma HepG2 cells

To investigate the antitumor activity of dehydrolovastatin and (or) cisplatin on HepG2 cells in vitro and to explore the possible molecular mechanisms, the inhibitory effect on cell proliferation, migration and invasion was evaluated by CCK-8 assay, cell colony formation assay, scratching assay and transwell assay after treated with dehydrolovastatin and (or) cisplatin. The expression of Rho A and MMP-2 genes and proteins were detected by real-time fluorescence quantitative PCR and Western blotting respectively. The results showed that Dehydrolovastatin inhibited the proliferation of HepG2 cells in a concentration-dependent manner. The IC50 value of dehydrolovastatin was 29.61umol/L on HepG2 cells after treatment for 48 hours, and the Q value of dehydrolovastatin combined with cisplatin was greater than or equal to 1.15 according to Kim's formula. The plate cloning experiment showed that dehydrolovastatin could significantly inhibit the formation of cell clone, the scratching assay showed that dehydrolovastatin inhibited the migration in a time-dependent manner, the results of transwell test showed that dehydrolovastatin could significantly reduce the number of transmembrane cells compared with the control group; the real-time fluorescence quantitative PCR and Western blot showed that dehydrolovastatin could down regulate the expression of MMP-2, RhoA genes and proteins respectively. In conclusion, Dehydrolovastatin could inhibit the ability of proliferation, migration and invasion, which might be associated with the regulation of the expression of migration related genes and proteins; the combination of lovastatin and cisplatin has synergistic antitumor effect on HepG2 cells.