Glucose metabolism and cancer

Curr Opin Cell Biol. 2006 Dec;18(6):598-608. doi: 10.1016/j.ceb.2006.10.005. Epub 2006 Oct 12.

Abstract

The first identified biochemical hallmark of tumor cells was a shift in glucose metabolism from oxidative phosphorylation to aerobic glycolysis. We now know that much of this metabolic conversion is controlled by specific transcriptional programs. Recent studies suggest that activation of the hypoxia-inducible factor (HIF) is a common consequence of a wide variety of mutations underlying human cancer. HIF stimulates expression of glycolytic enzymes and decreases reliance on mitochondrial oxidative phosphorylation in tumor cells, which occurs even under aerobic conditions. In addition, recent efforts have also connected the master metabolic regulator AMP-activated protein kinase (AMPK) to several human tumor suppressors. Several promising therapeutic strategies based on modulation of AMPK, HIF and other metabolic targets have been proposed to exploit the addiction of tumor cells to increased glucose uptake and glycolysis.

Publication types

  • Review

MeSH terms

  • AMP-Activated Protein Kinases
  • Animals
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Electron Transport Chain Complex Proteins / genetics
  • Energy Metabolism / physiology*
  • Glucose / metabolism*
  • Glycolysis / physiology
  • Humans
  • Hypoxia-Inducible Factor 1 / metabolism*
  • Multienzyme Complexes / metabolism
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Oxidative Phosphorylation
  • Protein-Serine-Threonine Kinases / metabolism

Substances

  • Electron Transport Chain Complex Proteins
  • Hypoxia-Inducible Factor 1
  • Multienzyme Complexes
  • Protein-Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • Glucose