Journal
NUCLEAR MEDICINE AND BIOLOGY
Volume 40, Issue 6, Pages 858-864Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.nucmedbio.2013.05.006
Keywords
AMP-activated protein kinase; Fluorodeoxyglucose; Hypoxia; Hypoxia-inducible factor 1; Oncology, Positron Emission Tomography
Funding
- Breast Cancer Campaign
Ask authors/readers for more resources
Introduction: Hypoxia can stimulate F-18-fluorodeoxyglucose (FDG) uptake in cultured cells. A better understanding of the underlying molecular mechanism is required to determine the value of FDG for studying tumour hypoxia. Methods: The effect of hypoxia on FDG uptake, and key proteins involved in glucose transport and glycolysis, was studied in MCF7 and MDA231 breast cancer cell lines. Results: Hypoxia induced a dose- and time-dependent increase in FDG uptake. The FOG increase was transient, suggesting that FDG uptake is only likely to be increased by acute hypoxia (<24 h). Molecular analysis indicated that hypoxia upregulated glut1 and 6-phosphofructo-2-kinase, key proteins involved in regulating glucose transport and glycolysis, and that these changes were induced by Hypoxia-Inducible factor 1 (HIF1) upregulation and/or AMP-activated protein kinase activation. Conclusions: FDG may provide useful information about the oxygenation status of cells in hypoxic regions where HIF1 upregulation is hypoxia-driven. (C) 2013 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available