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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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2017-06-01
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Series: | Frontiers in Oncology |
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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. |
first_indexed | 2024-04-12T21:45:37Z |
format | Article |
id | doaj.art-7656124c30a94342abe68f21bc66a9ee |
institution | Directory Open Access Journal |
issn | 2234-943X |
language | English |
last_indexed | 2024-04-12T21:45:37Z |
publishDate | 2017-06-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Oncology |
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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