The tumor suppressor function of mitochondria: Translation into the clinics

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1792

Review

Cuezva, Jose M.¹ 

[1] Univ Autonoma Madrid, CSIC, Ctr Biol Mol Severo Ochoa, Dept Biol Mol, E-28049 Madrid, Spain

关键词: Cancer;    Cell cycle;    Cell death;    Glycolysis;    H+-ATP synthase;    Markers of prognosis;    Metabolic inhibitor;    Oxidative phosphorylation;    ROS;   

DOI  :  10.1016/j.bbadis.2009.01.006

来源: Elsevier

【 摘 要 】

Recently, the inevitable metabolic reprogramming experienced by cancer cells as a result of the onset of cellular proliferation has been added to the list of hallmarks of the cancer cell phenotype. Proliferation is bound to the synchronous fluctuation of cycles of an increased glycolysis concurrent with a restrained oxidative phosphorylation. Mitochondria are key players in the metabolic cycling experienced during proliferation because of their essential roles in the transduction of biological energy and in defining the life-death fate of the cell. These two activities are molecularly and functionally integrated and are both targets of commonly altered cancer genes. Moreover, energetic metabolism of the cancer cell also affords a target to develop new therapies because the activity of mitochondria has an unquestionable tumor suppressor function. In this review, we summarize most of these findings paying special attention to the opportunity that translation of energetic metabolism into the clinics could afford for the management of cancer patients. More specifically, we emphasize the role that mitochondrial beta-F1-ATPase has as a marker for the prognosis of different cancer patients as well as in predicting the tumor response to therapy. (C) 2009 Elsevier B.V. All rights reserved.

【 授权许可】

Free