Oxidative Phosphorylation as a Target to Arrest Malignant Neoplasias

Author(s): Sara Rodriguez-Enriquez, Juan Carlos Gallardo-Perez, Alvaro Marin-Hernandez, Jose Luis Aguilar-Ponce, Edna Ayerim Mandujano-Tinoco, Abelardo Meneses, Rafael Moreno-Sanchez

Journal Name: Current Medicinal Chemistry

Volume 18 , Issue 21 , 2011

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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

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Article Details

Year: 2011
Page: [3156 - 3167]
Pages: 12
DOI: 10.2174/092986711796391561
Price: $65

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