Glucose metabolism in cancer cells

Curr Opin Clin Nutr Metab Care. 2010 Jul;13(4):466-70. doi: 10.1097/MCO.0b013e32833a5577.

Abstract

Purpose of review: Cancer cells alter their metabolism in order to support their rapid proliferation and expansion across the body. In particular, tumor cells, rather than fueling glucose in the oxidative phosphorylation pathway, generally use glucose for aerobic glycolysis. In this review, we discuss some of the mechanisms thought to be responsible for the acquisition of a glycolytic phenotype in cancer cells and how the switch towards glycolysis represents a selective growth advantage.

Recent findings: Glucose deprivation can activate oncogenes and these can upregulate proteins involved in aerobic glycolysis. In turn, proteins implicated in increased glycolysis can render tumor cells more resistant to apoptosis. Aerobic glycolysis induces acidification of the tumor environment, favoring the development of a more aggressive and invasive phenotype. Altering the pH around tumors might represent a way to hamper tumor development as suggested by a recent work demonstrating that bicarbonate, which increases the pH of tumors, prevented spontaneous metastatization.

Summary: The acquisition of a glycolytic phenotype by transformed cells confers a selective growth advantage to these cells. Interfering with aerobic glycolysis, therefore, represents a potentially effective strategy to selectively target cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aerobiosis / drug effects
  • Animals
  • Apoptosis
  • Bicarbonates / pharmacology*
  • Cell Proliferation / drug effects
  • Glucose / metabolism*
  • Glycolysis / drug effects
  • Humans
  • Hydrogen-Ion Concentration
  • Neoplasms / metabolism*
  • Oncogenes / physiology
  • Oxidative Phosphorylation / drug effects
  • Phenotype

Substances

  • Bicarbonates
  • Glucose