Study On The Effect Of Biological Behavior Induced By Sulforaphane And Mechanism In Gastric Cancer

Objective: Gastric cancer(GC)is a high incidence of human malignant tumors,and its incidence has been on the rise.In 2018,the number of cases and deaths of gastric cancer ranked second in China.Therefore,in-depth research on the treatment of gastric cancer is particularly important.Sulforaphane(SFN)is an isothiocyanate mainly derived from cruciferous vegetables such as broccoli,Brussels sprouts and cabbage.It can regulate many signal pathways in the organism.A large number of studies have confirmed that SFN plays an anti-tumor role in breast cancer,colon cancer,prostate cancer,bladder cancer and gastric cancer,but the potential mechanism of the anti-cancer activity of SFN is still not fully understood.The purpose of this study was to explore the effects of SFN on the cell cycle and apoptosis of BGC-823 and MGC-803 cells,and to explore its possible molecular mechanism.Methods: MTT method was used to detect the effect of SFN at different concentrations on the activity of BGC-823 and MGC-803 cell lines in 24,48 and 72hours;cell clone formation experiment was used to detect the effect of SFN on the proliferation of BGC-823 and MGC-803 cell lines;flow cytometry was used to detect the effect of SFN on the cell cycle of BGC-823 and MGC-803;Hoechst 33258 was used The effects of SFN on the apoptosis of BGC-823 and MGC-803 cells were detected by 33258 staining and flow cytometry;Western blot analysis of the effects of SFN on the expression of cell cycle-related proteins and apoptosis-related proteins such as CDK2,P53,P21,Bax,and Cleaved-caspase-3.Results: Compared with the blank control group,the exposure of SFN to the BGC-823 and MGC-803 cell lines caused damage to the cell viability and colonyforming ability: the cell activity of the SFN exposed group decreased,and the number of clones decreased significantly.In addition,SFN significantly inhibits cell proliferation by stopping the cell cycle in the S phase and enhancing the apoptosis of BGC-823 and MGC-803 cells in a dose-dependent manner.Western blot results showed that the treatment of BGC-823 and MGC-803 cells with SFN resulted in a significant increase in the expression of P53 and P21 associated with the S phase of the cell cycle and a decrease in the expression of CDK2.Bax and Cleaved-caspase-3involved in apoptosis Protein expression increased significantly in a dose-dependent manner.Conclusions: SFN can reduce the activity and inhibit the proliferation of gastric cancer cells,and its mechanism may induce S-phase cell cycle arrest by activating the P53-mediated P21-CDK2 axis in gastric cancer cells,and induce apoptosis through the P53-mediated mitochondrial apoptosis pathway.