Journal
CANCER JOURNAL
Volume 21, Issue 2, Pages 75-87Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PPO.0000000000000098
Keywords
Cancer; wound healing; hypoxia; tumor metabolism; glycolytic switch; angiogenic switch; Pasteur effect; Warburg effect; hypoxia-inducible factor 1 (HIF-1); lactate; monocarboxylate transporters (MCTs)
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Funding
- European Research Council [243188]
- Interuniversity Attraction Pole grant from the Belgian Science Policy Office (Belspo) [UP7-03]
- Communaute Francaise de Belgique [ARC 14/19-058]
- Belgian Fondation Contre le Cancer (Fundamental Research Grant) [F86]
- Belgian Fonds National de la Recherche Scientifique (F.R.S.-FNRS)
- Belgian Federal Agency for Nuclear Control (AFCN-FANC) [P.0. 4500020406]
- Fonds Joseph Maisin
- UCL Fonds Speciaux de la Recherche (FSR)
- Austrian Science Fund (FWF) [F86] Funding Source: Austrian Science Fund (FWF)
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Hypoxia is a characteristic of tumors and wounds. Hypoxic cells develop 2 common strategies to face hypoxia: the glycolytic switch and the angiogenic switch. At the onset of hypoxia, alleviation of the Pasteur effect ensures short-term cell survival. Long-term hypoxic cell survival requires a further acceleration of the glycolytic flux under the control of hypoxia-inducible factor 1 that stimulates the expression of most glycolytic transporters and enzymes, uncouples glycolysis from the TCA cycle, and rewires glycolysis to lactic fermentation. Hypoxic cells also trigger angiogenesis, a process that aims to restore normal microenvironmental conditions. Transcription factors (hypoxia-inducible factor 1, nuclear factor B, activator protein 1) and lactate cooperate to stimulate the expression of proangiogenic agents. Cancer cells differ from normal hypoxic cells by their proliferative agenda and by a high metabolic heterogeneity. These effects in tumor account for further molecular and metabolic changes and for a persistent stimulation of angiogenesis.
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