Experimental Study On Antitumor Effects And Its Mechanisms Of RASSF1A In A Hepatocellular Carcinoma Cell Line

Objective: The antitumor role of RASSF1A and its potential molecular mechanisms are not well understood. In this study, we tested this antitumor ability in hepatocellular carcinoma (HCC), and studied the mechanisms of cell growth and cell apoptosis induced by RAS SF1 A.Methods: After stably transfecting RASSF1A (wild type or mutant) expression vector into the HCC cell line QGY-7703, we tested the effects of RASSF1A reexpression on cell growth and proliferation, colony formation, tumorigenesis in nude mice, cell cycle, cell sensitivity to antitumor drug and the expression level of some related molecule.Results: Wild type RASSF1A, not the mutant, suppressed cell growth in vitro and in vivo, resulted in Gl/S cell cycle arrest, decreased the level of cyclin Dl protein which was likely at the level of posttranscriptional control. Although we did not find Ras expression had effect on RASSFlA-induced growth arrest, reexpression of wild type RASSF1A could enhance the cell inhibited rate and the percentage of apoptosis cells treated with mitomycin in the QGY-7703 cells.Conclusions: Wild type RASSF1A enhances cell sensitivity to mitomycin, and suppresses cell growth in vivo and in vitro through decreasing the level of cyclin Dl protein in HCC, suggesting that RASSF1A may serve as a new target for gene therapy for HCC.