Cited by 91Nitric Oxide and Endothelin EffectsInflammatory mediators and NSAID effectsRedox biology and oxidative stress

Inducible Nitric Oxide Synthase in the Carcinogenesis of Gastrointestinal Cancers

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de Oliveira, Graciele Almeida, Cheng, Robert Y.S., Ridnour, Lisa A., Basudhar, Debashree, Somasundaram, Veena, McVicar, Daniel W., Monteiro, Hugo Pequeno, Wink, David A.·2017·Antioxidants & Redox Signaling

Abstract

Significance: Gastrointestinal (GI) cancer taken together constitutes one of the most common cancers worldwide with a broad range of etiological mechanisms. In this review, we have examined the impact of nitric oxide (NO) on the etiology of colon, colorectal, gastric, esophageal, and liver cancers. Recent Advances: Despite differences in etiology, initiation, and progression, chronic inflammation has been shown to be a common element within these cancers showing interactions of numerous pathways. NO generated at the inflammatory site contributes to the initiation and progression of disease. The amount of NO generated, time, and site vary and are an important determinant of the biological effects initiated. Among the nitric oxide synthase enzymes, the inducible isoform has the most diverse range, participating in numerous carcinogenic processes. There is emerging evidence showing that inducible nitric oxide synthase (NOS2) plays a central role in the process of tumor initiation and/or development. Critical Issues: Redox inflammation through NOS2 and cyclooxygenase-2 participates in driving the mechanisms of initiation and progression in GI cancers. Future Directions: Understanding the underlying mechanism involved in NOS2 activation can provide new insights into important prevention and treatment strategies. Antioxid. Redox Signal. 26, 1059–1077.

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  • In higher organisms, NO is involved in cell signaling and maintenance of homeostasis, but high levels of this metabolite lead to chemical stress.

    “In higher organisms, NO is involved in cell signaling and maintenance of homeostasis, but high levels of this metabolite lead to chemical stress, possibly also contributing to the induction and progression of diseases [38,39].”

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Research works printed but not linked: 1

  1. Heath CW, Jr., Thun MJ, Greenberg ER, Levin B, and Marnett LJ. Nonsteroidal antiinflammatory drugs and human cancer. Report of an interdisciplinary research workshop. Cancer 74: 2885-2888, 1994.

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Authors
de Oliveira, G. A., Cheng, R. Y. S., Ridnour, L. A., Basudhar, D., Somasundaram, V., McVicar, D. W., Monteiro, H. P., & Wink, D. A.
Affiliations
  • National Institutes of Health
  • National Institutes of Health (US)
  • Universidade Federal de São Paulo (BR)
Corresponding author
Wink, David A.
Venue
Antioxidants & Redox Signaling
Published
2017-06
Volume
26
Issue
18
Pages
1059-1077
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
OpenAlex
W2501946307
Cited by
91
References
199
Citations by year
2026: 4 · 2025: 12 · 2024: 7 · 2023: 13 · 2022: 10 · 2021: 8 · 2020: 12 · 2019: 12 · 2018: 6 · 2017: 6 · 2016: 1
FWCI
0.98
Type
journal article
Language
en
Open access
Locations
  • Antioxidants and Redox Signaling (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • UNIFESP Institutional Repository (Universidade Federal de São Paulo) (submittedVersion)
Funders
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (2014‐0)
  • National Institutes of Health
  • Ciência sem Fronteiras
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
inducible nitric oxide synthase, NOS2, nitric oxide, gastrointestinal cancer, carcinogenesis, chronic inflammation, cyclooxygenase-2, colon cancer, colorectal cancer, gastric cancer, esophageal cancer, liver cancer, tumor initiation, tumor progression
MeSH terms
Animals, Gastrointestinal Neoplasms, Humans, Inflammation, Nitric Oxide, Oxidation-Reduction, Disease Progression, Cyclooxygenase 2, Nitric Oxide Synthase Type II, Carcinogenesis

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