RESUMEN
Gastric cancer is the third leading type of cancer and has the third leading cancerassociated mortality in China. The mechanism of thermochemotherapy in gastric cancer cells remains to be elucidated. The present study aimed to investigate the role of autophagic cell death in the thermochemotherapy of gastric cancer. The current study included four groups: An empty control group, a hyperthermia group, a chemotherapy (oxaliplatin) group, and a thermochemotherapy group. Cell viability was analyzed by the MTS assay. Production of intracellular reactive oxygen species (ROS) was quantified by flow cytometry. Autophagyassociated proteins, Beclin 1, microtubuleassociated protein 1A/1Blight chain (LC3B) and mammalian target of rapamycin (mTOR), were determined by western blot analysis. The results indicated that thermochemotherapy markedly increased intracellular ROS production, and decreased mitochondrial membrane potential. The transmission electron microscopy results indicated that thermochemotherapy induced production of autophagic bodies. In addition, thermochemotherapyinduced cell damage at the cellular and animal levels indicated a notable increase in the expression of the autophagyassociated genes, LC3B and Beclin 1. A negative correlation between mTOR expression and autophagy was also identified, which demonstrates that thermochemotherapy induces autophagic cell death by activating the autophagyassociated signaling pathways. The results of the present study demonstrated that the ROS level is important in autophagic death of the gastric carcinoma cells, and the increased ROS level, induced by thermochemotherapy treatment, induced autophagy in gastric carcinoma cells.