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Chemoprevention of Colon Cancer by iNOS-Selective Inhibitors

Naveena B Janakiram1, Chinthalapally V Rao

  • 1Center for Cancer Prevention and Drug Development, Medical Oncology, Department of Medicine, PCS Oklahoma Cancer Center, University of Oklahoma Health Sciences, Oklahoma City, Oklahoma.

Forum on Immunopathological Diseases and Therapeutics
|May 17, 2013
PubMed

Insights

Nitric oxide (NO), produced by inducible NO synthases (iNOS), plays a complex role in colon cancer. While it can promote tumor growth, high levels may induce cell death, suggesting therapeutic potential.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Nitric oxide (NO) is a critical regulator in immunity and cancer, produced from L-arginine by NO synthases (NOSs).
  • Inducible NOS (iNOS) overproduction during inflammation generates reactive NO intermediates, promoting DNA damage, altered cell signaling, and carcinogenesis.
  • Increased iNOS expression is observed in colorectal tumors, implicating NO in colon tumorigenesis via inflammatory cytokines and protein modifications.

Purpose of the Study:

  • To explore the dual role of nitric oxide (NO) in colon cancer development and progression.
  • To investigate the mechanisms by which NO influences tumor cell proliferation, invasion, and apoptosis.
  • To evaluate the potential of targeting iNOS and related pathways for colon cancer prevention.

Main Methods:

  • Review of existing literature on nitric oxide synthases (NOSs) and their role in cancer.
  • Analysis of signaling pathways involving NO, inflammation, and cell death in colorectal tumorigenesis.
  • Examination of experimental data on the effects of NO and its metabolites on tumor growth and invasion.

Main Results:

  • Sustained iNOS induction contributes to carcinogenesis by causing DNA damage and promoting pro-inflammatory and angiogenic properties.
  • NO signaling pathways in colon cancer involve inflammatory cytokines and post-translational modifications of antiapoptotic molecules.
  • NO can stimulate tumor proliferation, invasion, and migration, but high levels may induce tumor cell death.

Conclusions:

  • Nitric oxide (NO) exhibits a complex, context-dependent role in colon cancer, capable of both promoting and inhibiting tumor growth.
  • The interplay between NO, inflammation, and prostaglandin production (via cyclooxygenase-2) significantly influences colon tumorigenesis.
  • Targeting iNOS and cyclooxygenase-2 pathways offers a potential strategy for colon cancer prevention.
Keywords:
angiogenesischemopreventioncolorectal canceriNOS-selective inhibitorsnitric oxide

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