Lactylation in gastric cancer: From mechanisms to clinical applications (Review)

Gastric cancer (GC) is one of the most common malignant tumors worldwide. Metabolic reprogramming and epigenetic dysregulation represent its key pathological characteristics. As a novel lactate‑mediated post‑translational modification, lactylation converts metabolic signals into epigenetic and protein functional regulation, and it is extensively and aberrantly activated in GC. Lactylation drives the malignant progression of GC by promoting cell proliferation, invasion, metastasis and stemness. In addition, lactylation suppresses antitumor immune cell functions, and mediates immune escape and therapeutic resistance. Clinically, global lactylation levels and specific lactylation sites can serve as independent prognostic biomarkers, and corresponding risk models enable prognostic stratification and prediction of immunotherapy response. Intervention strategies targeting lactate production, lactyltransferases and downstream effector axes have emerged as promising directions for GC treatment. The present review summarizes the regulatory mechanisms, biological functions and clinical translational value of lactylation in GC, aiming to provide novel insights for precision diagnostics and therapeutics.