Journal
BIOCHEMICAL PHARMACOLOGY
Volume 92, Issue 1, Pages 164-171Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2014.08.026
Keywords
Autophagy; Mitochondria; NADPH; PARP-1; Sirtuin
Categories
Funding
- Assistance publique des hopitaux de Paris, France
- Action Lions Vaincre le Cancer, Luxembourg
- Associazione Italiana per la Ricerca sul Cancro (AIRC)
- European Commission (ArtForce)
- Agence National de la Recherche (ANR)
- Ligue Nationale contre le Cancer
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Association pour la Recherche sur le Cancer (ARC)
- LabEx Immuno-Oncologie
- Fondation de France
- Fondation Bettencourt-Schueller
- AXA Chair for Longevity Research
- Canceropelle Ile-de-France
- Paris Alliance of Cancer Research Institutes (PACRI)
- Cancer Research for Personalized Medicine (CARPEM)
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Increasing evidence indicates that cancer cells rewire their metabolism during tumorigenesis. The high intracellular levels of lactate and reactive oxygen species (ROS) generated during enhanced aerobic glycolysis and mitochondrial oxidative phosphorylation respectively led to oxidative stress. The detoxification of these accumulating metabolites and the equilibrium between reduced and oxidized nicotine adenine dinucleotide (NADH and NAD(+)) are two prominent mechanisms regulating redox status and hence energy homeostasis in tumors. Targeting both processes may thus be selectively cytotoxic for cancer cells. In this context, the impact of poly(ADP-ribose) polymerase (PARP) inhibitors, a class of anticancer agents employed for the treatment of DNA repair deficient tumors, on energy homeostasis and mitochondrial respiration regulation has potential clinical implications. Here we provide an overview of the metabolic reprogramming occurring in cancer cells and discuss the translational perspectives of targeting tumor metabolism and redox balance for antineoplastic therapy. (C) 2014 Elsevier Inc. All rights reserved.
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