Intracellular prooxidant activity of melatonin induces a survival pathway involving NF-κB activation

Silvia Cristofanon*, Francesco Uguccioni, Claudia Cerella, Flavia Radogna, Mario Dicato, Lina Ghibelli, Marc Diederich

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

52 Citations (Scopus)

Abstract

We have shown that melatonin exerts a prooxidant activity in U937 cells, a tumor human promonocytic cell line.1 Here we show that melatonin induces a strong canonical activation of NF-κB, inducing IκBα degradation and the consequential nuclear translocation of p50/p65 subunits. The timing of NF-κB activation overlaps with the timing of reactive oxygen species (ROS) production due to melatonin. Overexpression of dominant-negative IκB, which prevents a possible NF-κB activation, transformed melatonin in a proapoptotic molecule. These data indicate for the first time that melatonin can trigger NF-κB activation and might suggest a possible role for ROS induced by melatonin. Results indicate a possible involvement in the survival pathway of melatonin-generated ROS as secondary messengers.

Original languageEnglish
Title of host publicationNatural Compounds and Their Role in Apoptotic Cell Signaling Pathways
PublisherBlackwell Publishing Inc.
Pages472-478
Number of pages7
ISBN (Print)9781573317375
DOIs
Publication statusPublished - Aug 2009
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
Volume1171
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Melatonin
  • NF-κB
  • Reactive oxygen species
  • Survival

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