Objective To study the effect and mechanism of autophagy in gastric cancer cells induced by β-sitosterol in vivo and in vitro,providing experimental evidence for antitumor study of β-sitosterol on gastric cancer.Methods Human gastric cancer SGC-7901 cells were cultured in vitro.The control group was treated with phosphate buffer (PBS) only,and the experimental group was treated with different concentrations of β-sitosterol.Tetrazolium salt colorimetry (MTT) was used to detect the inhibitory effect of β-sitosterol on gastric cancer cells.Flow cytometry was used to detect the apoptotic effect of β-sitosterol on gastric cancer cells.Green fluorescent protein labeling (GFP) was used to detect the induction of autophagy by β-sitosterol.Western blot was used to detect the expression of signal pathway proteins phosphorylated phosphoinositid 3-kinase (p-PI3K),phosphorylated protein kinase B (p-AKT) and phosphorylated mammalian target of rapamycin (p-mTOR).The nude mice model of gastric cancer was established by SGC-7901 cells.β-sitosterol was injected abdominally once every 3 days for 42 days.The weight and volume of transplanted tumors were observed.The expression of LC3-Ⅱ and LC3-Ⅰ in transplanted tumors was detected by immunohistochemistry.Results β-sitosterol could inhibite the viability and promote the apoptosis of SGC-7901 cells,inducing the autophagy of SGC-7901 cells when its concentration reached 20 μmol/L.The autophagy rate of experimental group was (19.32 ±2.51,32.25 ±3.18,57.45 ±4.02,78.93 ±4.21),which was significantly higher than that in the control group (7.28 ± 2.83,P ＜ 0.05).In the experimental group,the expression of p-PI3K,p-AKT and mTOR was down-regulated by β-sitosterol,which was significantly different from that in the control group (P ＜ 0.05).The inhibition rate of the experimental group was (69.8 ± 3.6) ％,and the weight and volume of the transplanted tumors were significantly reduced compared with those in the control group (P ＜ 0.05).β-sitosterol increased the expression of LC3-Ⅱ,decreased expression of LC3-Ⅰ,leading the rise of ratio of LC3-Ⅱ to LC3-Ⅰ in nude mouse tumor (t =7.28,P =0.008).Conclusions β-sitosterol can inhibite proliferation and promote apoptosis of SGC-7901 cells.The antitumor mechanism may related to the autophagy induced by beta-sitosterol through PI3K/AKT/mTOR pathway.