Abstract: AIM: To study the effects of Se-methylselenocysteine(MSC) on the growth and apoptosis of human liver carcinoma cell line,HepG₂ cells and the molecular mechanism of effects.METHODS: After HepG₂ cells treated with various concentrations of MSC,survival and apoptosis were determined by MTT assay and light microscope,apoptosis and cell cycle were determined by flow cytometry.Malignant phenotype was determined by soft agarose growth assay.Cyclin D1 mRNA expression was determined by RT-PCR and Caspase-3 activity was measured by Caspase-3 activity assay kit.RESULTS: After being treated with 25 μmol·L^-1 MSC for 24 h,the survival of HepG₂ cells was decreased,a marked apoptosis and S phase arrest characteristic was observed in timeand dose- dependent manner.Soft agatose growth assay showed MSC inhibited HepG₂ cells growth in soft agarose.RT-PCR and Caspase-3 assay showed that HepG₂ cells treated with 25 μmol·L^-1 MSC for 24 and 48 hours,the expression of Cyclin D1 mRNA was down-regulated by 38% and 47%,while Caspase-3 activity was up-regulat-ed by (39.61±6.65)%and (118.73±6.48)%.Hep-G2 cells treated with 50 μmol·L^-1 MSC for 24 and 48 h,the expression of Cyclin D1 mRNA was down-regulated by 53% and 82%,whereas Caspase-3 activity was up-regulated by (80.66±9.31)% and (152.67±7.95)%.CONCLUSION: MSC can inhibit the growth of HepG₂ cells,and induce apoptosis and S phase arrest of HepG₂ cells.The phenotype alterations of HepG₂ cells might relate with inhibition of Cyclin D1 expression and Caspase-3activity by MSC in the cells.

Key words: Se-methylselenocysteine, HepG₂ cell, apoptosis, cell cycle, malignant phenotype