Redox signaling and cancer: the role of "labile" iron

Cancer Lett. 2008 Jul 18;266(1):21-9. doi: 10.1016/j.canlet.2008.02.038. Epub 2008 Apr 18.

Abstract

Reactive oxygen species (ROS) were viewed for a long time as unavoidable by-products of normal cell catabolism. This view has recently changed and it is now apparent that ROS generation is a tightly regulated process that plays a central role in cell signaling. Thus, it is known that regulated changes in intracellular ROS levels can induce biochemical signaling processes that control basic cellular functions, such as proliferation and apoptosis which are prevalent in the development of cancer. In this short review, we will try to provide a background to this emerging field by summarizing the biochemistry of ROS-mediated cell signaling and its relation to carcinogenesis. Special emphasis will be focused on the emerging role of the so called "labile" iron (the redox-active form of iron) in ROS-mediated signaling in relation to cancer development. It is tempting to speculate that elucidation of the exact molecular mechanisms that govern ROS-mediated regulation of cell signaling will provide the basis for development of new therapeutic strategies for cancer prevention and treatment.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptation, Biological
  • Cysteine / metabolism
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Iron / metabolism*
  • Mutation
  • Neoplasms / etiology
  • Neoplasms / metabolism*
  • Oxidation-Reduction
  • Oxidative Stress
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction*

Substances

  • Reactive Oxygen Species
  • Hydrogen Peroxide
  • Iron
  • Cysteine