Fig. 7
Energy metabolism in cancer. Cancer cells undergo metabolic reprogramming in their energy metabolism, characterized by enhanced glycolysis, glutamine metabolism, and FAO, but the TCA cycle and OXPHOS are suppressed. The activity of glycolysis-related transport proteins and enzymes such as GLUT, HK, PFK, PK, and LDH is increased. The activity of glutamine transporters and GLS is increased, catalyzing the production of glutamate for biosynthesis or energy synthesis. The expression of fatty acid transport proteins (CD36) and synthetic proteins (ACLY, ACC, FASN) is increased. However, the activity of key enzymes in the TCA cycle, such as IDH, SDH, FH, and MDH, is suppressed. A variety of signaling molecules undergo changes in expression during this process and regulate the energy metabolism of cancer cells. Overall, HIF1-α, KRAS, SALL4, c-MYC, PI3K/AKT, and mTOR, among others, play pro-oncogenic roles mainly by promoting glycolysis and glutaminolysis while inhibiting the TCA cycle and oxidative phosphorylation. P53, PTEN, AMPK, NRF2, PCG1α, and others play tumor-suppressive roles, inhibiting glycolysis and fatty acid transport and synthesis while promoting the mitochondrial TCA cycle and oxidative phosphorylation processes (red boxes: promoting signaling molecules; blue boxes: inhibitory signaling molecules). HK hexokinase, PFK phosphofructokinase, PK pyruvate kinase, ALDHO aldehyde dehydrogenase, GAPDH glyceraldehyde-3-phosphate dehydrogenase, PGK1 phosphoglycerate kinase 1, LDH lactate dehydrogenase, PDH pyruvate dehydrogenase, PDK1 pyruvate dehydrogenase kinase 1, ACLY ATP citrate lyase, ACC acetyl-CoA carboxylase, FASN fatty acid synthase, ACS acetyl-CoA synthase, GLS glutaminase, GDH glutamate dehydrogenase, IDH isocitrate dehydrogenase, SDH succinate dehydrogenase, FH fumarate hydratase, MDH malate dehydrogenase, CPT1 carnitine palmitoyltransferase 1
