TY - JOUR
T1 - The Biology of Cancer
T2 - Metabolic Reprogramming Fuels Cell Growth and Proliferation
AU - DeBerardinis, Ralph J.
AU - Lum, Julian J.
AU - Hatzivassiliou, Georgia
AU - Thompson, Craig B.
N1 - Funding Information:
The authors thank N. Thompson for work on the figures and members of the Thompson laboratory for critical reading of the manuscript. This work was supported by National Institutes of Health grants PO1 CA104838 (C.B.T.) and K08 DK072565 (R.J.D.) and the Damon Runyon Cancer Research Foundation (G.H.).
PY - 2008/1/9
Y1 - 2008/1/9
N2 - Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis.
AB - Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis.
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U2 - 10.1016/j.cmet.2007.10.002
DO - 10.1016/j.cmet.2007.10.002
M3 - Review article
C2 - 18177721
AN - SCOPUS:37449024702
SN - 1550-4131
VL - 7
SP - 11
EP - 20
JO - Cell Metabolism
JF - Cell Metabolism
IS - 1
ER -