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NF-kappaB activation prevents apoptotic oxidative stress via an increase of both thioredoxin and MnSOD levels in TNFalpha-treated Ewing sarcoma cells.

Author information

Affiliations

  • 1. INSERM U365, Institut Curie, Section de recherche, 26 rue d'Ulm, 75248 Paris cedex 05, France.
      Authors
    • Djavaheri-Mergny M 1
    (1 author)

ORCIDs linked to this article

FEBS Letters, 01 Dec 2004, 578(1-2):111-115
https://doi.org/10.1016/j.febslet.2004.10.082 PMID: 15581626 

Abstract 

Repression of activation of c-Jun N-terminal kinase (JNK) participates in the anti-apoptotic effect of nuclear factor-kappaB (NF-kappaB) in TNFalpha-treated Ewing sarcoma cells. As oxidative stress is one of the most prominent activators of JNK, we investigated the relationship between TNFalpha-induced NF-kappaB activation and the control of oxidative stress. Inhibition of NF-kappaB activation resulted in an increase in TNFalpha-induced ROS production, lipid peroxidation and protein oxidation. Those ROS and lipid peroxides were both involved in TNFalpha-induced apoptosis, whereas only ROS elevation triggered sustained JNK activation. TNFalpha increased the level of two antioxidant enzymes, thioredoxin and manganese superoxide dismutase by an NF-kappaB-dependent mechanism. Inhibition of expression or activity of these enzymes sensitized cells to TNFalpha-induced apoptosis, indicating their functional role in protection from cell death. Thus, agents that inhibit activities of these enzymes may prove helpful in the treatment of Ewing tumors.

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Read article at publisher's site: https://doi.org/10.1016/j.febslet.2004.10.082

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