Inducible Nitric Oxide Synthase in the Carcinogenesis of Gastrointestinal Cancers
Open accessAbstract
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].”
From Known Antimicrobials Versus Nortriptyline in Candida albicans: Repositioning an Old Drug for New Targets (2020) · cites this paper as [39]
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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.
- ORCID
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2017-06
- Volume
- 26
- Issue
- 18
- Pages
- 1059-1077
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC5488308
- 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
- hybrid
- doi.org
- Licence
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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