Tumor necrosis factor-associated protein 1 (TRAP-1) protects cells from oxidative stress and apoptosis

N. Montesano Gesualdi, G. Chirico, G. Pirozzi, E. Costantino, M. Landriscina, F. Esposito

Research output: Contribution to journalArticlepeer-review


TRAP-1 is a mitochondrial heat shock protein (HSP), recently identified in Saos-2 osteosarcoma cells adapted to mild oxidative stress induced by diethylmaleate (DEM). TRAP-1 mRNA expression is increased in DEM-adapted cells as well as in tumor cells resistant to 5-fluorouracil and to platin derivatives. Since a strong decrease of TRAP-1 protein levels, upon cisplatin treatment, is observed only in controls but not in the DEM-adapted counterpart, a possible role for this protein in the development of resistant phenotypes could be hypothesized. To characterize the protective role of TRAP-1 against oxidative stress and apoptosis, stable transfectants were generated and characterized for their response to different stress types. These stable clones expressing constitutively high TRAP-1 levels: (i) are more resistant to H2O2-induced DNA damage and to apoptosis by cisplatin; (ii) contain higher reduced glutathione (GSH) levels than control cells; and (iii) do not release the apoptosis-inducing factor into the nucleus upon cisplatin treatment. Furthermore, high TRAP-1 levels interfere with caspase 3 activation. These results confirm the anti-apoptotic role of TRAP-1, and suggest that increased expression of this mitochondrial HSP in DEM-adapted and chemoresistant cells could be part of a pro-survival signaling pathway aimed to evade toxic effects of oxidants and anticancer drugs.

Original languageEnglish
Pages (from-to)342-350
Number of pages9
Issue number4
Publication statusPublished - Nov 2007


  • Apoptosis
  • Chemoresistance
  • Heat shock protein 75
  • Osteosarcoma
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology


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