Glucose metabolism reprogramming in gastric cancer: Implications for tumor

Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, with advanced stages often showing limited therapeutic response and frequent drug resistance. Growing evidence underscores glucose metabolism reprogramming as a pivotal mechanism promoting tumor progression, immune evasion, and treatment resistance in GC. However, the mechanistic details and clinical relevance of metabolic rewiring in GC remain insufficiently elucidated. This review comprehensively analyzes recent advances in glucose metabolic reprogramming in GC, covering key enzymes, transporters, non-coding RNAs, and metabolites involved in glycolysis, gluconeogenesis, the pentose phosphate pathway, and glucose uptake. By synthesizing current evidence, we highlight clinically relevant mechanisms such as lactate-mediated immunosuppression-via polarization of Tregs and M2 macrophages-and metabolic adaptations that drive chemotherapy resistance. Our findings provide a mechanistic basis for targeting glucose metabolism to overcome drug resistance, suppress metastasis, and enhance immunotherapy efficacy in GC. Thus, targeting metabolic reprogramming represents a promising strategy for developing personalised therapies and improving outcomes in GC patients. Further translational and clinical studies are urgently needed to validate these metabolic pathways as therapeutic targets.