AI Article Synopsis
- The Warburg hypothesis suggested that cancer cells rely primarily on glycolysis for energy due to mitochondrial damage, but this theory may not hold true for all types of tumors.
- Researchers have found that despite high glycolytic activity, many cancer cells actually produce most of their ATP through oxidative phosphorylation.
- The review suggests that targeting mitochondrial metabolism with specific drug therapies could effectively complement existing treatments for cancers that depend on oxidative phosphorylation for energy.
Article Abstract
Since Warburg proposed in 1956 that cancer cells exhibit increased glycolysis due to mitochondrial damage, numerous researchers have assumed that glycolysis is the predominant ATP supplier for cancer cell energy-dependent processes. However, chemotherapeutic strategies using glycolytic inhibitors have been unsuccessful in arresting tumor proliferation indicating that the Warburg hypothesis may not be applicable to all existing neoplasias. This review analyzes recent information on mitochondrial metabolism in several malignant neoplasias emphasizing that, although tumor cells maintain a high glycolytic rate, the principal ATP production may derive from active oxidative phosphorylation. Thus, anti-mitochondrial drug therapy may be an adequate adjuvant strategy to arrest proliferation of oxidative phosphorylation-dependent neoplasias.
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| http://dx.doi.org/10.2174/092986711796391561 | DOI Listing |
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