Abstract: Objective　To explore the effect of quercetin (QE) on gastric cancer-related p53/AMPK/mTOR signaling pathway. Methods　Gastric cancer cells were divided into the QE group and the solvent group. DMSO was used as the solvent. QE was formulated into 0.02 (QEA group), 0.04 (QEB group), 0.06 (QEC group), and 0.08 mmol/L (QED group) solutions. The solvent group was added the same amount of solvent without QE. MTT test was used to detect the effect of quercetin on gastric cancer cell proliferation. MDC staining method was used to detect the effect of quercetin on gastric cancer cell autophagy. Double staining method was used to detect the effect of quercetin on gastric cancer cell apoptosis. Real-time polymerase chain reaction test was used to detect the relative expression levels of p53, AMPK and mTOR mRNA in cells. Western blot assay was used to detect the differences in the expression levels of LC3Ⅱ/LC3Ⅰ, P53, AMPK and mTOR in cells. Results　Compared with the solvent group, the autophagy and apoptosis rate of gastric cancer cells were significantly increased in the different QE dose groups (P＜0.05). The expression of LC3Ⅱ/LC3Ⅰ protein in cells was up-regulated in the QE groups, and p53, AMPK mRNA and protein levels were also up-regulated, and the mRNA and protein expression of mTOR were down-regulated (P＜0.05) with a dose-dependent pattern. Conclusion　Quercetin can inhibit the proliferation of gastric cancer cells, induce autophagy and promote apoptosis, which may be related to the p53/AMPK/mTOR signaling pathway.

Key words: Quercetin, stomach neoplasms, autophagy, apoptosis, p53/AMPK/mTOR signaling pathway