TY - JOUR AB - Helicobacter pylori (H. pylori) is a gram‑negative pathogen that colonizes gastric epithelial cells. The drug resistance rates of H. pylori have dramatically increased, causing persistent infections. Chronic infection by H. pylori is a critical cause of gastritis, peptic ulcers and even gastric cancer. In host cells, autophagy is stimulated to maintain cellular homeostasis following intracellular pathogen recognition by the innate immune defense system. However, H. pylori‑induced autophagy is not consistent during acute and chronic infection. Therefore, a deeper understanding of the association between H. pylori infection and autophagy in gastric epithelial cells could aid the understanding of the mechanisms of persistent infection and the identification of autophagy‑associated therapeutic targets for H. pylori infection. The present review describes the role of H. pylori and associated virulence factors in the induction of autophagy by different signaling pathways during acute infection. Additionally, the inhibition of autophagy in gastric epithelial cells during chronic infection was discussed. The present review summarized H. pylori‑mediated autophagy and provided insights into its mechanism of action, suggesting the induction of autophagy as a novel therapeutic target for persistent H. pylori infection. AD - Department of Oncology Surgery, Lanzhou University Second Hospital, Lanzhou, Gansu 730030, P.R. China AU - Zhang,Fan AU - Chen,Cong AU - Hu,Jike AU - Su,Ruiliang AU - Zhang,Junqiang AU - Han,Zhijian AU - Chen,Hao AU - Li,Yumin DA - 2019/12/01 DO - 10.3892/ol.2019.10976 EP - 6227 IS - 6 JO - Oncol Lett KW - Helicobacter pylori autophagy stomach neoplasms vacuolating cytotoxin cytotoxin‑associated gene A PY - 2019 SN - 1792-1074 1792-1082 SP - 6221 ST - Molecular mechanism of Helicobacter pylori‑induced autophagy in gastric cancer (Review) T2 - Oncology Letters TI - Molecular mechanism of Helicobacter pylori‑induced autophagy in gastric cancer (Review) UR - https://doi.org/10.3892/ol.2019.10976 VL - 18 ER -