Redox signaling in cancer biology

Antioxid Redox Signal. Jul-Aug 2006;8(7-8):1249-52. doi: 10.1089/ars.2006.8.1249.


Over the last three decades, it is has become increasing clear that intracellular signaling pathways are activated via changes in intracellular metabolic oxidation/reduction (redox) reactions involving reactive oxygen species (ROS; i.e., superoxide and hydrogen peroxide). The initial proposals hypothesized that signaling through metabolic oxidation/reduction (redox) reactions involving ROS could contribute to carcinogenesis and progression to malignancy. Strong evidence for this hypothesis was obtained from studies showing that environmental insults (i.e., ionizing radiation) as well as xenobiotics (i.e., polycyclic aromatic hydrocarbons and phorbol esters) capable of inducing steady-state increases in free radical production and ROS could act as both initiators and promoters of carcinogenesis. This Forum is directed at understanding possible redox signaling mechanisms governing cellular radiation response, tumor growth, and response to therapy, as well as the role of nitric oxide in cancer biology.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Free Radicals / metabolism
  • Humans
  • Neoplasms / etiology
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Nitric Oxide / metabolism
  • Oxidation-Reduction / drug effects
  • Oxidation-Reduction / radiation effects
  • Radiation, Ionizing
  • Reactive Nitrogen Species / metabolism
  • Reactive Oxygen Species / metabolism
  • Signal Transduction*
  • Xenobiotics / pharmacology


  • Free Radicals
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Xenobiotics
  • Nitric Oxide