Fig. 8

Diagram of the mechanisms underlying glucose transporter (GLUT) 3 regulation of lactylation in gastric cancer. To satisfy the energy needs of tumor proliferation and progression, gastric cancer cells accelerate glucose intake and increase energy metabolism. To that end, they highly express GLUTs to achieve a high glucose oxidation rate, which results in the generation and accumulation of large amounts of lactate. Excess lactate acts as a precursor for histone lactylation, which triggers gastric cancer cell epithelial–mesenchymal transition, and promotes gastric cancer invasiveness and metastasis