RASSF1A expression inhibits cell growth and enhances cell chemosensitivity to mitomycin in BEL-7402 hepatocellular carcinoma cells

Background The antitumor role of Ras association domain family 1A (RASSF1A) gene and its potential molecularmechanisms are not well understood.The objective of this study was to observe the antitumor ability of RASSF1A inhepatocellular carcinoma,and study the mechanisms of cell apoptosis induced by RASSF1A.Methods After stably transfecting a RASSF1A (wild-type or mutant) expression vector into the BEL-7402 hepatocellularcarcinoma cell line,RT-PCR and Western blotting was used to detect the RASSF1A expression levels in recombinantcells.The effects of wild-type RASSF1A on cell growth were observed in vitro by analyzing cell proliferation rate,cellcolony formation,and in vivo by analyzing tumorigenesis in nude mice.In addition,the effect of RASSF1A geneexpression on the chemosensitivity of human hepatocellular carcinoma cells to antitumor drugs was examined byinhibition of cell proliferation and the percentage of apoptotic cells.Results Wild-type RASSF1A,not the mutant,suppressed cell growth in vitro and in vivo.Re-expression of wild-typeRASSF1A could enhance the inhibition of cell proliferation and the percentage of apoptotic cells following cell treatment withmitomycin,but had no significant effect when combined with adriamycin,etoposide,5-fluorouracil and cisplatin treatment.Conclusion Wild-type RASSF1A inhibits cell growth and enhances cell chemosensitivity to mitomycin in hepatocellularcarcinoma,suggesting that RASSF1A may serve as a new target for gene therapy in hepatocellular carcinomapatients.