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Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics


Affiliations
1 Inserm UMR-S 1172, Universite de Lille, 59045 Place Verdun Cedex, France
2 Centre Hospitalier Regional et Universitaire (CHRU) de Lille, 5900 Lille, France
 

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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  • Integration of Mitochondrial Targeting for Molecular Cancer Therapeutics

Abstract Views: 68  |  PDF Views: 0

Authors

Philippe Marchetti
Inserm UMR-S 1172, Universite de Lille, 59045 Place Verdun Cedex, France
Pierre Guerreschi
Inserm UMR-S 1172, Universite de Lille, 59045 Place Verdun Cedex, France
Laurent Mortier
Centre Hospitalier Regional et Universitaire (CHRU) de Lille, 5900 Lille, France
Jerome Kluza
Inserm UMR-S 1172, Universite de Lille, 59045 Place Verdun Cedex, France

Abstract


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.