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Trends Cell Biol. 2014 Aug;24(8):455-63. doi: 10.1016/j.tcb.2014.03.005. Epub 2014 Apr 11.

Mitochondrial oxidative phosphorylation TRAP(1)ped in tumor cells.

Author information

1
CNR Institute of Neuroscience, University of Padova, 35121 Padova, Italy; Department of Biomedical Sciences, University of Padova, 35121 Padova, Italy. Electronic address: rasola@bio.unipd.it.
2
Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
3
Department of Cell Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.

Abstract

Many tumors undergo a dramatic metabolic shift known as the Warburg effect in which glucose utilization is favored and oxidative phosphorylation is downregulated, even when oxygen availability is plentiful. However, the mechanistic basis for this switch has remained unclear. Recently several independent groups identified tumor necrosis factor receptor-associated protein 1 (TRAP1), a mitochondrial molecular chaperone of the heat shock protein 90 (Hsp90) family, as a key modulator of mitochondrial respiration. Although all reports agree that this activity of TRAP1 has important implications for neoplastic progression, data from the different groups only partially overlap, suggesting that TRAP1 may have complex and possibly contextual effects on tumorigenesis. In this review we analyze these recent findings and attempt to reconcile these observations.

KEYWORDS:

ROS; TRAP1; cancer metabolism; chaperones; mitochondria

PMID:
24731398
DOI:
10.1016/j.tcb.2014.03.005
[Indexed for MEDLINE]

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