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The Warburg effect in tumor cells involves the uptake of high levels of glucose, enhanced glycolysis, and the metabolism of pyruvate to lactic acid rather than oxidative phos-phorylation to generate energy under aerobic conditions. This effect is closely related to the occurrence, invasion, metastasis, drug resistance, and poor prognosis of gastric cancer (GC). Current research has further demonstrated that the Warburg effect in GC cells is not only mediated by the glycolysis pathway, but also includes roles for mitochondria, noncoding RNAs, and other proteins that do not directly regulate metabolism. As a result, changes in the glycolysis pathway not only lead to abnormal glucose metabolism, but they also affect mitochondrial functions, cellular processes such as apoptosis and cell cycle regulation, and the metabolism of lipids and amino acids. In this review, we discuss metabolic reprogramming in GC based on glycolysis, a possible link between glucose metabolism, lipid metabolism, and amino acid metabolism, and we clarify the role of mitochondria. We also examine recent studies of metabolic inhibitors in GC.
Liu et al. (Fri,) studied this question.