CagA regulates autophagy through PI3K/AKT/mTOR pathway. (A) Expression of p-Akt(Ser473), Akt, p-mTOR, mTOR, p-S6, S6, MAP1LC3B-I, and MAP1LC3B-II in AGS cells infected with Hp-WT or Hp-ΔcagA(MOI = 100) at different time points. (B) Expression of p-Akt(Ser473), Akt, p-mTOR, mTOR, p-S6, S6, MAP1LC3B-I, and MAP1LC3B-II in AGS cells transfected with GFP-CagA, GFP-CagA-Mut or control plasmid. (C) Expression of p-Akt(Ser473), Akt, p-mTOR, mTOR, p-S6, S6, MAP1LC3B-I, and MAP1LC3B-II in AGS cells transfected c-Met siRNA or control siRNA (50 nM) for 24 h and then infected with Hp-WT or Hp-ΔcagA (MOI = 100) for 6 h. (D) Expression of p-Akt(Ser473), Akt, p-mTOR, mTOR, p-S6, S6, MAP1LC3B-I, and MAP1LC3B-II in AGS cells infected with Hp-WT or Hp-ΔcagA (MOI = 100) for 6 h with or without pre-treatment of MK-2206 (8 μM). (E) Production of IL-8, IL-1β and TNF-α in AGS cells transfected c-Met siRNA or control siRNA (50 nM) for 24 h and then infected with Hp-WT or Hp-ΔcagA (MOI = 100) for 6 h, as assessed by ELISA. (F) After pretreatment of DMSO or MK-2206 (8 μM), AGS cells were infected with Hp-WT or Hp-ΔcagA (MOI = 100:1) for 6 h. Supernatants were assessed by ELISA for levels of IL-8, IL-1β, and TNF-α. Experiments performed in triplicate showed consistent results. *P < 0.05.