The Mitochondrial Complex(I)ty of Cancer

Recent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH–ubiquinone oxidoreductase (Complex I) is the largest comp...

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Main Authors: Félix A. Urra, Felipe Muñoz, Alenka Lovy, César Cárdenas
Format: Article
Language:English
Published: Frontiers Media S.A. 2017-06-01
Series:Frontiers in Oncology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fonc.2017.00118/full
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author Félix A. Urra
Félix A. Urra
Felipe Muñoz
Felipe Muñoz
Alenka Lovy
César Cárdenas
César Cárdenas
César Cárdenas
César Cárdenas
author_facet Félix A. Urra
Félix A. Urra
Felipe Muñoz
Felipe Muñoz
Alenka Lovy
César Cárdenas
César Cárdenas
César Cárdenas
César Cárdenas
author_sort Félix A. Urra
collection DOAJ
description Recent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH–ubiquinone oxidoreductase (Complex I) is the largest complex of the mitochondrial electron transport chain and contributes about 40% of the proton motive force required for mitochondrial ATP synthesis. In addition, Complex I plays an essential role in biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Although knowledge about the structure and assembly of Complex I is increasing, information about the role of Complex I subunits in tumorigenesis is scarce and contradictory. Several small molecule inhibitors of Complex I have been described as selective anticancer agents; however, pharmacologic and genetic interventions on Complex I have also shown pro-tumorigenic actions, involving different cellular signaling. Here, we discuss the role of Complex I in tumorigenesis, focusing on the specific participation of Complex I subunits in proliferation and metastasis of cancer cells.
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spelling doaj.art-7656124c30a94342abe68f21bc66a9ee2022-12-22T03:15:38ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2017-06-01710.3389/fonc.2017.00118261887The Mitochondrial Complex(I)ty of CancerFélix A. Urra0Félix A. Urra1Felipe Muñoz2Felipe Muñoz3Alenka Lovy4César Cárdenas5César Cárdenas6César Cárdenas7César Cárdenas8Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Santiago, ChileGeroscience Center for Brain Health and Metabolism, Santiago, ChileAnatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Santiago, ChileGeroscience Center for Brain Health and Metabolism, Santiago, ChileDepartment of Neuroscience, Center for Neuroscience Research, Tufts School of Medicine, Boston, MA, United StatesAnatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Santiago, ChileGeroscience Center for Brain Health and Metabolism, Santiago, ChileThe Buck Institute for Research on Aging, Novato, CA, United StatesDepartment of Chemistry and Biochemistry, University of California, Santa Barbara, Santa Barbara, CA, United StatesRecent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH–ubiquinone oxidoreductase (Complex I) is the largest complex of the mitochondrial electron transport chain and contributes about 40% of the proton motive force required for mitochondrial ATP synthesis. In addition, Complex I plays an essential role in biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Although knowledge about the structure and assembly of Complex I is increasing, information about the role of Complex I subunits in tumorigenesis is scarce and contradictory. Several small molecule inhibitors of Complex I have been described as selective anticancer agents; however, pharmacologic and genetic interventions on Complex I have also shown pro-tumorigenic actions, involving different cellular signaling. Here, we discuss the role of Complex I in tumorigenesis, focusing on the specific participation of Complex I subunits in proliferation and metastasis of cancer cells.http://journal.frontiersin.org/article/10.3389/fonc.2017.00118/fullelectron transport chainmitochondrial respirationcancer cellsmetastasisanticancer agents
spellingShingle Félix A. Urra
Félix A. Urra
Felipe Muñoz
Felipe Muñoz
Alenka Lovy
César Cárdenas
César Cárdenas
César Cárdenas
César Cárdenas
The Mitochondrial Complex(I)ty of Cancer
Frontiers in Oncology
electron transport chain
mitochondrial respiration
cancer cells
metastasis
anticancer agents
title The Mitochondrial Complex(I)ty of Cancer
title_full The Mitochondrial Complex(I)ty of Cancer
title_fullStr The Mitochondrial Complex(I)ty of Cancer
title_full_unstemmed The Mitochondrial Complex(I)ty of Cancer
title_short The Mitochondrial Complex(I)ty of Cancer
title_sort mitochondrial complex i ty of cancer
topic electron transport chain
mitochondrial respiration
cancer cells
metastasis
anticancer agents
url http://journal.frontiersin.org/article/10.3389/fonc.2017.00118/full
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