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The considerable death rates and lack of symptoms in early stages of gastric cancer (GC) make it a major health problem worldwide. One of the most prominent risk factors is infection with Helicobacter pylori. Many biological processes, including those linked with cell death, are disrupted in GC. The cellular "self-digestion" mechanism necessary for regular balance maintenance, autophagy, is at the center of this disturbance. Misregulation of autophagy, however, plays a role in the development of GC. In this review, we will examine how autophagy interacts with other cell death processes, such as apoptosis and ferroptosis, and how it affects the progression of GC. In addition to wonderful its role in the epithelial-mesenchymal transition, it is engaged in GC metastasis. The role of autophagy in GC in promoting drug resistance stands out. There is growing interest in modulating autophagy for GC treatment, with research focusing on natural compounds, small-molecule inhibitors, and nanoparticles. These approaches could lead to breakthroughs in GC therapy, offering new hope in the fight against this challenging disease. [Display omitted] • Aberrant activation of autophagy in gastric cancer (GC) changes proliferation and metastasis. • Autophagy dysregulation affects the response of GC cells to chemotherapy. • Small molecules, natural compounds and nanomaterials regulate autophagy in GC therapy. • The autophagy-related factors can be considered as diagnostic and prognostic factors in GC. • Autophagy shows interaction with apoptosis and ferroptosis in GC. [ABSTRACT FROM AUTHOR]