Bodine Journal

Article Title

Control of Glycolytic Flux by AMPK and p53-Mediated Signaling Pathways in Tumor Cells Adapted to Grow at Low pH

Authors

E. E. Mendoza, University of ArizonaFollow
J. Caro, Thomas Jefferson University and HospitalsFollow
D. B. Leeper, Thomas Jefferson University and HospitalsFollow
R. Burd, University of ArizonaFollow

Abstract

Introduction: Tumor cells grow in nutrient and oxygen deprived microenvironments and adapt to the suboptimal growth conditions by altering metabolic pathways. This adaptation process characteristically results in a tumor phenotype that displays anaerobic glycolysis, chronic acidification and aggressive tumor characteristics. Understanding the tumor cell reaction to the microenvironment is a critical factor in predicting the tumor response to hyperthermia. The glucose regulatory molecule, 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase Isoform-3 (PFKFB3), is a bifunctional enzyme central to glycolytic flux and downstream of the metabolic stress sensor AMP-activated protein kinase (AMPK), which has been shown to activate an isoform of Phosphofructokinase (PFK-2).

Society for Thermal Medicine Annual Meeting April 23-26, Clearwater Beach, FL.

Recommended Citation

Mendoza, E. E.; Caro, J.; Leeper, D. B.; and Burd, R. (2010) "Control of Glycolytic Flux by AMPK and p53-Mediated Signaling Pathways in Tumor Cells Adapted to Grow at Low pH," Bodine Journal: Vol. 3: Iss. 1, Article 4.
DOI: https://doi.org/10.29046/TBJ.003.1.003
Available at: https://jdc.jefferson.edu/bodinejournal/vol3/iss1/4