Antiproliferative Activity And Mechanism Of Ailanthone On SGC-7901 Human Gastric Cancer Cells

Objective:To investigate the antitumor effects of ailanthone on SGC-7901 cells,and to analyze its underlying molecular mechanisms.Methods:The SGC-7901 cells were treated with ailanthone of different concentration（0.5-8μmol/L）or taxol of different concentration（1.25-20μmol/L）for 24,48 and 72 h,respectively.Control cells were treated with DMSO（0.1%）,without ailanthone and taxol.Then CCK-8 was used to detect the antiproliferative activities of ailanthone and taxol on SGC-7901 cells.The Hoechst 33258 staining was used to observe the apoptotic morphology of cells treated with ailanthone for 48h.The apoptosis and cell cycle progress of cells were measured by flow cytometry.The protein and mRNA expression levels of Bcl-2 and Bax were detected by western-blot analysis and reverse transcription-quantitative polymerase chain reaction（RT-qPCR）,respectively.Results:Following treatment with ailanthone or taxol,the results of CCK-8 indicated that ailanthone and taxol inhibited the proliferation of cells in a dose-and time-dependent manner.The half maximal inhibitory concentration(IC₅₀)values of ailanthone at 24,48 and 72 h were 5.473,2.906 and 2.47μmol/L in SGC-7901 cells respectively,and the IC₅₀ value of taxol at 24h was 14.47μmol/L in SGC-7901 cells.Compared with control cells,the characteristic apoptotic morphology,including nuclear shrinkage and chromatin,were more observed in the cells treated with ailanthone at the concentration of 1 and 2μmol/L for 48h.The results of flow cytometry analysis indicated that ailanthone could induce apoptosis and G2/M phase cell cycle arrest of SGC-7901 cells.Furthermore,analysis of the underlying molecular mechanisms revealed that ailanthone could downregulate the expression levels of Bcl-2,whereas the expression levels of Bax were upregulated at the protein and mRNA levels.Conclusion:Ailanthone may inhibit the growth of SGC-7901cells by inducing G2/M phase cell cycle aresst,and apoptosis via alteration of Bcl-2 and Bax in protein and mRNA expression levels.