Table 1.
Metabolic effects of the main proteins in cancer cells. Adapted with permission from Valle-Mendiola and Soto-Cruz [27].
| Protein | Expression in Cancer | Effects on the Metabolism |
|---|---|---|
| Pyruvate kinase isoform M2 (Isoform embryonic) | Increased expression in tumors and cancer cell lines | Increased glycolysis |
| Monocarboxylate transporters (MCTs) | Overexpressed in ovarian, prostate, gastric, and cervical cancers | Increased glycolysis |
| Glutaminase and glutamate oxaloacetate transaminases | Increased expression in cancer | Use of glutamine as a source of ATP and generation of TCA intermediaries |
| Via PI3K/Akt | Dysregulated in cancer | Increased glycolysis |
| HIF-1α | Overexpressed in cancer | Increased glycolysis |
| Myc | Dysregulated in cancer | Promotes the use of glutamine, glycolysis augmented |
| p53 | Mutated in cancer (inactivated) | Active p53 inhibits glycolysis and promotes oxidative phosphorylation. Loss of p53, increased glycolysis |
| Phosphofruct kinase/fructose-2,6-biphosphatase gene B3 (six isoforms) | Augmented expression | Increased glycolytic flux |
| Hexokinase II | Increased expression in hepatoma, cervical cancer | Increased glycolysis |
| Phosphofruct kinase 1 | Hyperactivated in cancer | Increased glycolysis |
| Pyruvate dehydrogenase kinase (PDK, four isoforms) | Increased in cancer | Increased glycolysis |
| Snail (E-cadherin repressor) | Increases epithelial–mesenchymal transition | Suppresses oxidative metabolism in mitochondria |
| Kisspeptin | Cancer metastasis suppressor of thyroid, ovary, bladder, gastric, esophageal, pancreatic, lung, pituitary, and melanoma | Promotes oxidative metabolism, inhibiting glycolysis |