Abstract
The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes. For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro. In research published in Cell and Bioscience, Jiang and colleagues show that pharmacological restriction of glucose metabolism decreases tumor progression in a TSC xenograft model.See research article: http://www.cellandbioscience.com/content/1/1/34
Highlights
The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes
Most differentiated cells primarily metabolize glucose to carbon dioxide by oxidation of pyruvate in the mitochondrial tricarboxylic acid (TCA) cycle, a process known as oxidative phosphorylation that requires far less glucose to generate the same amount of energy
In normal cells the switch from a non-proliferating state, in which oxidative phosphorylation meets the cell’s energy needs, to proliferation, in which glycolysis domi nates, is triggered by growth factors acting through the mammalian Target of Rapamycin Complex 1 signaling pathway (Figure 1)
Summary
The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes. In normal cells the switch from a non-proliferating state, in which oxidative phosphorylation meets the cell’s energy needs, to proliferation, in which glycolysis domi nates, is triggered by growth factors acting through the mammalian Target of Rapamycin Complex 1 (mTORC1) signaling pathway (Figure 1).
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