Abstract: Objective To explore the effects of dehydrocostus lactone (DHCL) on autophagy, apoptosis, and oxidative stress of gastric cancer cell line SGC-7901. Methods SGC-7901 cells cultured in vitro were divided into 0, 10, 20, and 40 μmol / L DHCL groups. Cell proliferation was analyzed by CCK-8 assays. Autophagic activity was assessed by immunofluorescence. Apoptosis was detected by flow cytometry. The levels of superoxide dismutase ( SOD ), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) in culture supernatants were detected by ELISA. The level of intracellular reactive oxygen species (ROS) was detected by the DCFH-DA probe. Expression of LC3-I, LC3-II, Beclin-1, autophagy-associated protein 7 (ATG7), p62, B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), BH3 interaction domain death agonist ( Bid), truncated Bid, Caspase-8, Caspase-9, Caspase-3, cleaved Caspase-8, cleaved Caspase-9, and cleaved Caspase-3 were detected by Western blot. A 0. 2 mL suspension of SGC-7901 cells (1× 107 / mL) was implanted subcutaneously. After intraperitoneal injection of 20 mg / (kg·d) DHCL for 2 weeks, tumor tissues were weighed. Results Cell survival rates in 40 and 20 μmol / L DHCL groups were lower than that in the 0 μmol / L DHCL group (P<0.05). In comparison with the 0 μmol / L DHCL group, autophagy and the apoptosis rate were higher in the 40 μmol / L and 20 μmol / L DHCL group (P<0.05). SOD and GSH-Px levels were lower than in the 0 μmol / L DHCL group (P<0.05). MDA and ROS levels were higher than in the 0 μmol / L DHCL group (P<0.05). Expression of p62 protein was lower in the 0 μmol / L DHCL group. Expression of Beclin-1, LC3II/ LC3I, ATG7, Bax / Bcl-2, tBid / Bid, cleaved Caspase-8/ Caspase-8, cleaved Caspase-9/ Caspase-9, and cleaved Caspase-3/ Caspase-3 was higher in the 0 μmol / L DHCL group (P<0.05). The nude mouse tumorigenicity assay showed that the weight of transplanted tumors in the DHCL group was lower than that in the control group (P<0.05). Conclusions DHCL promotes production of ROS in SGC-7901 cells and induces autophagic death and apoptosis.