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Mol. Cell. Biol. 21 (17): 5899-5912

Copyright © 2001 by the American Society for Microbiology. All rights reserved.

Molecular and Cellular Biology, September 2001, p. 5899-5912, Vol. 21, No. 17
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.17.5899-5912.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Growth Factors Can Influence Cell Growth and Survival through Effects on Glucose Metabolism

Matthew G. Vander Heiden,1,2 David R. Plas,1,2 Jeffrey C. Rathmell,1,2 Casey J. Fox,1,2 Marian H. Harris,1,2 and Craig B. Thompson1,2,*

Abramson Family Cancer Research Institute1 and Department of Cancer Biology,2 University of Pennsylvania, Philadelphia, Pennsylvania 19104

Received 30 November 2000/Returned for modification 2 February 2001/Accepted 25 May 2001

Cells from multicellular organisms are dependent upon exogenous signals for survival, growth, and proliferation. The relationship among these three processes was examined using an interleukin-3 (IL-3)-dependent cell line. No fixed dose of IL-3 determined the threshold below which cells underwent apoptosis. Instead, increasing growth factor concentrations resulted in progressive shortening of the G1 phase of the cell cycle and more rapid proliferative expansion. Increased growth factor concentrations also resulted in proportional increases in glycolytic rates. Paradoxically, cells growing in high concentrations of growth factor had an increased susceptibility to cell death upon growth factor withdrawal. This susceptibility correlated with the magnitude of the change in the glycolytic rate following growth factor withdrawal. To investigate whether changes in the availability of glycolytic products influence mitochondrion-initiated apoptosis, we artificially limited glycolysis by manipulating the glucose levels in the medium. Like growth factor withdrawal, glucose limitation resulted in Bax translocation, a decrease in mitochondrial membrane potential, and cytochrome c redistribution to the cytosol. In contrast, increasing cell autonomous glucose uptake by overexpression of Glut1 significantly delayed apoptosis following growth factor withdrawal. These data suggest that a primary function of growth factors is to regulate glucose uptake and metabolism and thus maintain mitochondrial homeostasis and enable anabolic pathways required for cell growth. Consistent with this hypothesis, expression of the three genes involved in glucose uptake and glycolytic commitment, those for Glut1, hexokinase 2, and phosphofructokinase 1, was found to rapidly decline to nearly undetectable levels following growth factor withdrawal.


* Corresponding author. Mailing address: Abramson Family Cancer Research Institute, 450 BRB II, 421 Curie Blvd., Philadelphia, PA 19104. Phone: (215) 746-5515. Fax: (215) 746-5511. E-mail: drt{at}mail.med.upenn.edu.


Molecular and Cellular Biology, September 2001, p. 5899-5912, Vol. 21, No. 17
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.17.5899-5912.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

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RACK1 Is an Insulin-like Growth Factor 1 (IGF-1) Receptor-interacting Protein That Can Regulate IGF-1-mediated Akt Activation and Protection from Cell Death.
P. A. Kiely, A. Sant, and R. O'Connor (2002)
J. Biol. Chem. 277, 22581-22589
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Genotoxic Exposure Is Associated with Alterations in Glucose Uptake and Metabolism.
R. Zhou, M. G. Vander Heiden, and C. M. Rudin (2002)
Cancer Res. 62, 3515-3520
   Abstract »    Full Text »    PDF »
Human Cytomegalovirus Major Immediate-Early Proteins and Simian Virus 40 Large T Antigen Can Inhibit Apoptosis through Activation of the Phosphatidylinositide 3'-OH Kinase Pathway and the Cellular Kinase Akt.
Y. Yu and J. C. Alwine (2002)
J. Virol. 76, 3731-3738
   Abstract »    Full Text »    PDF »
Increased Hexokinase Activity, of Either Ectopic or Endogenous Origin, Protects Renal Epithelial Cells against Acute Oxidant-induced Cell Death.
J. M. Bryson, P. E. Coy, K. Gottlob, N. Hay, and R. B. Robey (2002)
J. Biol. Chem. 277, 11392-11400
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Mitochondrial Binding of Hexokinase II Inhibits Bax-induced Cytochrome c Release and Apoptosis.
J. G. Pastorino, N. Shulga, and J. B. Hoek (2002)
J. Biol. Chem. 277, 7610-7618
   Abstract »    Full Text »    PDF »
Cells and More Cells: The American Society for Cell Biology Washington, DC December 8-12, 2001.
R. Tuma and W. A. Wells (2002)
J. Cell Biol. 156, 220-226
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IL-7 Enhances the Survival and Maintains the Size of Naive T Cells.
J. C. Rathmell, E. A. Farkash, W. Gao, and C. B. Thompson (2001)
J. Immunol. 167, 6869-6876
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