Glucose Metabolism in Cancer and Ischemia: Possible Therapeutic Consequences of the Warburg Effect
Language English Country United States Media print-electronic
Document type Journal Article, Review, Research Support, Non-U.S. Gov't
- MeSH
- Adrenergic beta-Antagonists pharmacology MeSH
- Glucose metabolism MeSH
- Glycolysis MeSH
- Ischemia drug therapy metabolism MeSH
- Dichloroacetic Acid pharmacology MeSH
- Humans MeSH
- Neoplasms drug therapy metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Adrenergic beta-Antagonists MeSH
- Glucose MeSH
- Dichloroacetic Acid MeSH
The Warburg effect states that the main source of energy for cancer cells is not aerobic respiration, but glycolysis-even in normoxia. The shift from one to the other is governed by mutually counteracting enzymes: pyruvate dehydrogenase and pyruvate dehydrogenase kinase (PDK). Anaerobic metabolism of cancer cells promotes cell proliferation, local tissue immunosuppression, resistance to hypoxic conditions, and metastatic processes. By switching glucose back to oxidative metabolism, these effects might be reversed. This can be achieved using PDK inhibitors, such as dichloroacetate. Patients suffering from ischemic conditions might benefit from this effect. On the other hand, the β-blockers (adrenergic β-antagonists) often used in these patients appear to improve cancer-specific survival, and nonselective β-blockers have been shown to promote glucose oxidation. Might there be a link?
b Medical Faculty University of Ljubljana Ljubljana Slovenia
e Weill Cornell Medicine in Qatar Qatar Foundation Education City Doha Qatar
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