To explore the mechanism of deguelin(De) in inducing apoptosis of gastric cancer cells SGC-7901.Methods:The cytotoxicity of De at different concentrations(10,20,40,60,80,and 100 mol/L) for 24 and 48 h to SGC-7901 cells was investigated by cell counting kit-8(CCK-8) cell viability assay.SGC-7901 cells were divided into a control group and 20 and 40 mol/L De groups.After 24 h of administration,the expression levels of phosphor-protein kinase B(p-AKT)Thr308,forkhead box O1(FoxO1),and B-cell lymphoma-2(Bcl-2) proteins were determined by Western blot.AKT gene transfection was used to make the high expression of AKT in SGC-7901 cells.Then,20 and 40 mol/L of De were given for 24 h,and SGC-7901 cells that were not transfected with the AKT gene were used as the control group.Meanwhile,Western blot was used to determine the protein expression levels of p-AKTThr308,FoxO1,and Bcl-2,and real-time quantitative polymerase chain reaction(RT-qPCR) was used to determine the mRNA expression levels of FoxO1,Bcl-2,and Bcl-2 associated X protein(Bax).Results:Different concentrations of De showed certain cytotoxicity to gastric cancer cells SGC-7901.The 20 and 40 mol/L of De significantly decreased the protein expression levels of p-AKTThr308 and Bcl-2 in SGC-7901 cells,and increased the level of FoxO1 after treatment for 24 h.As compared with the control group,the protein expression levels of p-AKTThr308 and Bcl-2 in SGC-7901 cells were increased and FoxO1 was decreased after AKT gene transfection.As compared with the model group,the protein expression levels of p-AKTThr308 and Bcl-2 and the mRNA expression level of Bcl-2 were decreased,and the expression levels of FoxO1 and Bax were increased after treatment with 20 and 40 mol/L of De.Conclusion:De can induce the apoptosis of gastric cancer cells SGC-7901 by acting on the AKT/FoxO1 signaling pathway.