Role of autophagy in gastric carcinogenesis

Figure 1 Autophagy activity pattern in normal and gastric malignant cells. Under normal conditions autophagy is strictly regulated in response to stimuli to preserve cytoplasm homeostasis. Excessive downregulation promotes gastric carcinogenesis and upon malignant transformation, the autophagic over activity contributes to progression, metastasis and negative prognosis. H. pylori: Helicobacter pylori.

Figure 2 The role of autophagy in normal and malignant gastric cells in response to specific stimuli. Normal stomach cell-related autophagy appears to inhibit oncogenesis and preserve homeostasis, whereas its downregulation facilitates malignant transformation. Gastric cancer cells express autophagy promoters to yield their energy supplementation, and thus progression, metastasis, negative overall survival and chemoresistance. Several autophagy inhibitors have been recognized to act against malignant cells, thus representing promising targets for future therapeutics. ATGs: Autophagy-related genes; DAPK3: Death-associated protein kinase 3; CagA: Cytotoxin-associated gene A; H. pylori: Helicobacter pylori; miR: MicroRNA; SIRT: Sirtuin; VacA: Vacuolating cytotoxin.