Oxidative Stress, Inflammation, and Cancer: How Are They Linked?

Free Radic Biol Med. 2010 Dec 1;49(11):1603-16. doi: 10.1016/j.freeradbiomed.2010.09.006. Epub 2010 Sep 16.

Abstract

Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked.

Publication types

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

MeSH terms

  • Animals
  • Cell Proliferation
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Drug Resistance, Neoplasm / genetics
  • Drug Resistance, Neoplasm / immunology
  • Humans
  • Inflammation / complications*
  • Inflammation / etiology
  • Inflammation / genetics
  • Inflammation / pathology
  • Models, Biological
  • Neoplasms / blood supply
  • Neoplasms / etiology*
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Neovascularization, Pathologic / etiology
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / pathology
  • Oxidative Stress / genetics
  • Oxidative Stress / physiology*
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • Tumor Escape / genetics
  • Tumor Escape / immunology