Portal:CPTAC/Hallmark/Deregulating
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| + | To fuel uncontrolled cell proliferation, cancer cells adjust energy metabolism. First observed by Otto Warburg, even in the presence of oxygen, cancer cells can reprogram their glucose metabolism, and thus their energy production, by limiting their energy metabolism largely to glycolysis, leading to a state that has been termed “aerobic glycolysis.” To compensate for the lower efficiency of ATP production by glycolysis, as compared to oxidative phosphorylation, cancer cells compensate, for example by up-reglating glucose transporters. (Adapted from [https://www.ncbi.nlm.nih.gov/pubmed/21376230 Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011]) | ||
*[[Pathway:WP2868]] TCA Cycle Nutrient Utilization and Invasiveness of Ovarian Cancer | *[[Pathway:WP2868]] TCA Cycle Nutrient Utilization and Invasiveness of Ovarian Cancer | ||
*[[Pathway:WP1471]] Target Of Rapamycin (TOR) Signaling | *[[Pathway:WP1471]] Target Of Rapamycin (TOR) Signaling | ||
Current revision
To fuel uncontrolled cell proliferation, cancer cells adjust energy metabolism. First observed by Otto Warburg, even in the presence of oxygen, cancer cells can reprogram their glucose metabolism, and thus their energy production, by limiting their energy metabolism largely to glycolysis, leading to a state that has been termed “aerobic glycolysis.” To compensate for the lower efficiency of ATP production by glycolysis, as compared to oxidative phosphorylation, cancer cells compensate, for example by up-reglating glucose transporters. (Adapted from Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011)
- Pathway:WP2868 TCA Cycle Nutrient Utilization and Invasiveness of Ovarian Cancer
- Pathway:WP1471 Target Of Rapamycin (TOR) Signaling
- Pathway:WP534 Glycolysis and Gluconeogenesis
- Pathway:WP143 Fatty Acid Beta Oxidation
- Pathway:WP4206 Hereditary Leiomyomatosis and Renal Cell Carcinoma Pathway
- Pathway:WP4290 Metabolic reprogramming in colon cancer
