Exosomes and extracellular vesicles in gastric cancer immune escape.

Gastric cancer (GC) remains a major cause of cancer-related mortality, largely due to late-stage diagnosis and the emergence of primary or acquired resistance to standard chemotherapies. Increasing evidence identifies extracellular vesicles (EVs), particularly exosomes, as central mediators of intercellular communication within the tumor microenvironment (TME). Extracellular vesicles (EVs) represent a heterogeneous population of membrane-bound particles that include exosomes, microvesicles, and apoptotic bodies, which differ in size, biogenesis, and functional properties. In this review, the term EVs is used as a comprehensive definition, while exosomes are referred to as a specific subtype originating from the endosomal pathway. Tumor-derived exosomes enriched in proteins, lipids, and nucleic acids profoundly reprogram infiltrating immune cells, shaping a highly immunosuppressive niche that supports tumor progression. In GC, exosomal immune checkpoint ligands, oncogenic non-coding RNAs, and vesicle remodeling driven by Helicobacter pylori infection collectively rewire immune surveillance, fostering a permissive microenvironment that sustains tumor growth and therapeutic resistance. At the clinical level, circulating EVs are emerging as powerful liquid-biopsy tools, supporting early detection, prognostic classification, and the prediction of responses to immune checkpoint inhibitors. Here, we discuss current insights into EV biogenesis and cargo sorting in GC, delineate how EVs reshape anti-tumor immunity and promote immune escape, and explore the translational potential of targeting EVs or their cargos as innovative therapeutic strategies in this aggressive malignancy.