Effects of small extracellular vesicles, autophagy and their crosstalk on the progression of gastric cancer.

Small extracellular vesicles (sEVs), which transport signaling molecules, facilitate communication among cancer, immune, and endothelial cells within the tumor microenvironment (TME), influencing immune responses and tumor angiogenesis. sEVs significantly affect gastric cancer (GC) development by transporting signaling molecules such as proteins and non-coding RNAs (ncRNAs). Autophagy plays a dual role in GC development; initially, it inhibits GC onset, but as the tumor progresses, it facilitates tumor growth by helping cancer cells adapt to stress and extend survival. Autophagy is intricately connected to sEVs biology and, more specifically, to exosome biogenesis, degradation, formation, and release through multiple mechanisms. At the same time, sEVs regulate autophagy-related signaling pathways in target cells by delivering bioactive cargoes that alter autophagy levels, which is particularly important in GC development. This article explores sEVs biogenesis, autophagy, and their interactions, providing additional molecular targets for the clinical diagnosis, treatment, and prognosis of GC.