ArticleJournal of experimental & clinical cancer research : CR2026
Extracellular vesicle-mediated GALNT1/RPRD1A glycosylation axis drives immune escape and peritoneal metastasis in gastric cancer.
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPeritoneal metastasis represents one of the most lethal clinical manifestations of gastric cancer (GC) and is closely associated with immune evasion. Extracellular vesicles (EVs) have emerged as critical mediators of tumor-immune communication; however, the molecular mechanisms by which EV-associated glycosylation regulates immune escape and metastatic dissemination remain largely undefined.
methodsEVs derived from highly metastatic GC cells were isolated and functionally characterized in vitro and in humanized immune system mouse models. Their clinical relevance was evaluated using paired human GC specimens. Underlying mechanisms were investigated through genetic manipulation, lectin-based glycosylation assays, and immune cell co-culture experiments.
resultsWe identified GALNT1 as an EV-enriched glycosyltransferase that promotes GC cell invasion and suppresses CD8
conclusionsThese findings identify an EV-driven GALNT1/RPRD1A glycosylation axis as a previously unrecognized mechanism underlying immune escape and peritoneal metastasis in GC and support this pathway as a potential therapeutic target for advanced disease.
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