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.
Keywords: Anti-mitochondrial drugs, glycolysis, oxidative phosphorylation, Warburg hypothesis, multi-site therapy, multi-drug therapy, respiratory inhibitors, uncouplers, lipophilic cation drugs, mitochondrial substrate oxidation, Krebs cycle
Current Medicinal Chemistry
Title: Oxidative Phosphorylation as a Target to Arrest Malignant Neoplasias
Volume: 18 Issue: 21
Author(s): Sara Rodriguez-Enriquez, Juan Carlos Gallardo-Perez, Alvaro Marin-Hernandez, Jose Luis Aguilar-Ponce, Edna Ayerim Mandujano-Tinoco, Abelardo Meneses and Rafael Moreno-Sanchez
Affiliation:
Keywords: Anti-mitochondrial drugs, glycolysis, oxidative phosphorylation, Warburg hypothesis, multi-site therapy, multi-drug therapy, respiratory inhibitors, uncouplers, lipophilic cation drugs, mitochondrial substrate oxidation, Krebs cycle
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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Rodriguez-Enriquez Sara, Carlos Gallardo-Perez Juan, Marin-Hernandez Alvaro, Luis Aguilar-Ponce Jose, Ayerim Mandujano-Tinoco Edna, Meneses Abelardo and Moreno-Sanchez Rafael, Oxidative Phosphorylation as a Target to Arrest Malignant Neoplasias, Current Medicinal Chemistry 2011; 18 (21) . https://dx.doi.org/10.2174/092986711796391561
DOI https://dx.doi.org/10.2174/092986711796391561 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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