TY - JOUR
T1 - Targeting mitochondria for cancer therapy
AU - Fulda, Simone
AU - Galluzzi, Lorenzo
AU - Kroemer, Guido
N1 - Funding Information:
We apologize to all colleagues whose articles we were unable to cite due to space limitations. We are indebted to O. Kepp for help in figure preparation. S.F. is supported by the Deutsche Forschungsgemeinschaft, the Deutsche Krebshilfe, the Bundesministerium für Bildung und Forschung, Wilhelm-Sander-Stiftung, Else-Kröner-Fresenius Stiftung, the Novartis Stiftung für therapeutische Forschung, the European Union (ApopTrain, APO-SYS), and IAP6/18. G.K. is supported by the Ligue Nationale contre le cancer (équipe labellisée), Agence National de Recherche (ANR), Cancéropôle Ile-de-France, Institut National du Cancer (INCa), Fondation pour la Recherche Médicale (FRM), and the European Union (Active p53, ApopTrain, APO-SYS, ChemoRes, TransDeath, RIGHT).
PY - 2010/6/1
Y1 - 2010/6/1
N2 - Mitochondria are the cells' powerhouse, but also their suicidal weapon store. Dozens of lethal signal transduction pathways converge on mitochondria to cause the permeabilization of the mitochondrial outer membrane, leading to the cytosolic release of pro-apoptotic proteins and to the impairment of the bioenergetic functions of mitochondria. The mitochondrial metabolism of cancer cells is deregulated owing to the use of glycolytic intermediates, which are normally destined for oxidative phosphorylation, in anabolic reactions. Activation of the cell death machinery in cancer cells by inhibiting tumour-specific alterations of the mitochondrial metabolism or by stimulating mitochondrial membrane permeabilization could therefore be promising therapeutic approaches.
AB - Mitochondria are the cells' powerhouse, but also their suicidal weapon store. Dozens of lethal signal transduction pathways converge on mitochondria to cause the permeabilization of the mitochondrial outer membrane, leading to the cytosolic release of pro-apoptotic proteins and to the impairment of the bioenergetic functions of mitochondria. The mitochondrial metabolism of cancer cells is deregulated owing to the use of glycolytic intermediates, which are normally destined for oxidative phosphorylation, in anabolic reactions. Activation of the cell death machinery in cancer cells by inhibiting tumour-specific alterations of the mitochondrial metabolism or by stimulating mitochondrial membrane permeabilization could therefore be promising therapeutic approaches.
UR - http://www.scopus.com/inward/record.url?scp=77953131908&partnerID=8YFLogxK
U2 - 10.1038/nrd3137
DO - 10.1038/nrd3137
M3 - Review article
C2 - 20467424
AN - SCOPUS:77953131908
SN - 1474-1776
VL - 9
SP - 447
EP - 464
JO - Nature Reviews Drug Discovery
JF - Nature Reviews Drug Discovery
IS - 6
ER -