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Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics

Mitochondrial metabolism greatly influences cancer cell survival, invasion, metastasis, and resistance to many anticancer drugs. Furthermore, molecular-targeted therapies (e.g., oncogenic kinase inhibitors) create a dependence of surviving cells on mitochondrial metabolism. For these reasons, inhibi...

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Detalles Bibliográficos
Autores principales: Marchetti, Philippe, Guerreschi, Pierre, Mortier, Laurent, Kluza, Jerome
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4680051/
https://www.ncbi.nlm.nih.gov/pubmed/26713093
http://dx.doi.org/10.1155/2015/283145
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author Marchetti, Philippe
Guerreschi, Pierre
Mortier, Laurent
Kluza, Jerome
author_facet Marchetti, Philippe
Guerreschi, Pierre
Mortier, Laurent
Kluza, Jerome
author_sort Marchetti, Philippe
collection PubMed
description Mitochondrial metabolism greatly influences cancer cell survival, invasion, metastasis, and resistance to many anticancer drugs. Furthermore, molecular-targeted therapies (e.g., oncogenic kinase inhibitors) create a dependence of surviving cells on mitochondrial metabolism. For these reasons, inhibition of mitochondrial metabolism represents promising therapeutic pathways in cancer. This review provides an overview of mitochondrial metabolism in cancer and discusses the limitations of mitochondrial inhibition for cancer treatment. Finally, we present preclinical evidence that mitochondrial inhibition could be associated with oncogenic “drivers” inhibitors, which may lead to innovative drug combinations for improving the efficacy of molecular-targeted therapy.
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spelling pubmed-46800512015-12-28 Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics Marchetti, Philippe Guerreschi, Pierre Mortier, Laurent Kluza, Jerome Int J Cell Biol Review Article Mitochondrial metabolism greatly influences cancer cell survival, invasion, metastasis, and resistance to many anticancer drugs. Furthermore, molecular-targeted therapies (e.g., oncogenic kinase inhibitors) create a dependence of surviving cells on mitochondrial metabolism. For these reasons, inhibition of mitochondrial metabolism represents promising therapeutic pathways in cancer. This review provides an overview of mitochondrial metabolism in cancer and discusses the limitations of mitochondrial inhibition for cancer treatment. Finally, we present preclinical evidence that mitochondrial inhibition could be associated with oncogenic “drivers” inhibitors, which may lead to innovative drug combinations for improving the efficacy of molecular-targeted therapy. Hindawi Publishing Corporation 2015 2015-12-02 /pmc/articles/PMC4680051/ /pubmed/26713093 http://dx.doi.org/10.1155/2015/283145 Text en Copyright © 2015 Philippe Marchetti et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Marchetti, Philippe
Guerreschi, Pierre
Mortier, Laurent
Kluza, Jerome
Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title_full Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title_fullStr Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title_full_unstemmed Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title_short Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics
title_sort integration of mitochondrial targeting for molecular cancer therapeutics
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4680051/
https://www.ncbi.nlm.nih.gov/pubmed/26713093
http://dx.doi.org/10.1155/2015/283145
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