Hypoxia stimulates 18F-Fluorodeoxyglucose uptake in breast cancer cells via hypoxia inducible factor-1 and AMP-activated protein kinase

Tim A. D. Smith, Matteo Zanda, Ian N. Fleming

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Introduction
Hypoxia can stimulate 18F-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 FDG 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.
Original languageEnglish
Pages (from-to)858-864
Number of pages7
JournalNuclear Medicine and Biology
Volume40
Issue number6
DOIs
Publication statusPublished - Aug 2013

Keywords

  • AMP-activated protein kinase
  • fluorodeoxyglucose
  • hypoxia
  • hypoxia-inducible factor 1
  • oncology
  • positron emission tomography

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