Fig. 1.

Lactate from aerobic glycolysis and glutaminolysis in cancer cells. Aerobic glycolysis in cancer cells is efficient because of the cytoplasmic regeneration of NAD⁺ from NADH by LDHA without participating in mitochondrial electron transport chain. Without this process, deficiency of NAD⁺ pool limits glycolysis of cancer cells, then decreasing the rate of glycolysis at the GAPDH-mediated step. The continuous activation of HIF-1α, c-Myc, and the mTOR pathway induces aberrant expression of multiple glycolytic enzymes, thus facilitating aerobic glycolysis in cancer cells. ASCT2, alanine/serine/cysteine transporter 2; GLUT1, glucose transporter 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; HIF-1α, hypoxia-inducible factor 1α; PFK-1, phosphofructokinase-1; MCT4, monocarboxylate transporter 4; mTOR, mechanistic target of rapamycin; LDHA, lactate dehydrogenase A. This figure is created by Pei Zhang, Zi-Hao Wang, and Qiong Zhou. All authors confirm originality of it and retain copyright to it.