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Oxidative Phosphorylation as a Target to Arrest Malignant Neoplasias

[ Vol. 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   Pages 3156 - 3167 ( 12 )

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

Affiliation:

Departamento de Bioquimica, Instituto Nacional de Cardiologia, Juan Badiano No. 1, Col. Seccion 16, Tlalpan, Mexico D.F. 14080, Mexico.



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