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