Journal
FRONTIERS IN ONCOLOGY
Volume 7, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2017.00058
Keywords
tumor necrosis factor receptor-associated protein 1; tumor metabolism; heat shock proteins; mitochondria; reactive oxygen species; post-translational modifications; kinase; allosteric ligands
Categories
Funding
- Associazione Italiana Ricerca sul Cancro [IG15863, IG15420]
- Children's Tumor Foundation (Drug Discovery Initiative Award) [2016A-05-009]
- Young Investigator Award of the Children's Tumor Foundation
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Mitochondria can receive, integrate, and transmit a variety of signals to shape many biochemical activities of the cell. In the process of tumor onset and growth, mitochondria contribute to the capability of cells of escaping death insults, handling changes in ROS levels, rewiring metabolism, and reprograming gene expression. Therefore, mitochondria can tune the bioenergetic and anabolic needs of neoplastic cells in a rapid and flexible way, and these adaptations are required for cell survival and proliferation in the fluctuating environment of a rapidly growing tumor mass. The molecular bases of pro-neoplastic mitochondrial adaptations are complex and only partially understood. Recently, the mitochondrial molecular chaperone TRAP1 (tumor necrosis factor receptor associated protein 1) was identified as a key regulator of mitochondrial bioenergetics in tumor cells, with a profound impact on neoplastic growth. In this review, we analyze these findings and discuss the possibility that targeting TRAP1 constitutes a new antitumor approach.
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