Warburg Effect is the observation that most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria like most normal cells
Several functions of p53 reduce the flux through the glycolytic pathway and increase oxidative phosphorylation, thereby opposing the Warburg effect, in which cancer cells predominantly use glycolysis for energy production. However, there are also activities of p53, such as the activation of hexokinase and phosphoglycerate mutase (PGM), which could increase glycolysis under some circumstances. GLUT, glucose transporter; IKK, IkappaB kinase; NF-kappaB, nuclear factor-kappaB; SCO2, synthesis of cytochrome c oxidase 2; TCA, tricarboxylic acid.
p53 and metabolism 2009
Glucose is shown transported across the plasma membrane. Hypoxia-inducible factor 1 (HIF1) and MYC collaborate to activate hexokinase 2 (HK2) and pyruvate dehydrogenase kinase 1 (PDK1), resulting in enhanced conversion of glucose to lactic acid. HIF1 and MYC independently activate the glucose transporter GLUT1 and lactate dehydrogenase A (LDHA). All of this contributes to the Warburg effect. PDH, pyruvate dehydrogenase; ROS, reactive oxygen species.
The interplay between MYC and HIF in cancer 2008
Modeling WE
Glycolysis
