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Published on: July 20, 2019
Induced nitric oxide synthase as a major player in the oncogenic transformation of inflamed tissue
Guang-Yu Yang1, Sofia Taboada, Jie Liao
1Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Abstract:
Nitric oxide (NO) is a free radical that is involved in the inflammatory process and carcinogenesis. There are four nitric oxide synthase enzymes involved in NO production: induced nitric oxide synthase (iNOS), endothelial NO synthase (eNOS), neural NO synthase (nNOS), and mitochondrial NOS. iNOS is an inducible and key enzyme in the inflamed tissue. Recent literatures indicate that NO as well as iNOS and eNOS can modulate cancer-related events including nitro-oxidative stress, apoptosis, cell cycle, angio-genesis, invasion, and metastasis. This chapter focuses on linking NO/iNOS/eNOS to inflammation and carcinogenesis from experimental evidence to potential targets on cancer prevention and treatment.
Insights
Nitric oxide (NO) and its producing enzymes, induced nitric oxide synthase (iNOS) and endothelial NO synthase (eNOS), play roles in inflammation and cancer. Understanding these links offers potential cancer prevention and treatment strategies.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Research
Background:
- Nitric oxide (NO) is a free radical implicated in inflammation and carcinogenesis.
- Four nitric oxide synthase (NOS) enzymes (iNOS, eNOS, nNOS, mitochondrial NOS) produce NO.
- Induced nitric oxide synthase (iNOS) is a key enzyme in inflamed tissues.
Purpose of the Study:
- To link nitric oxide (NO), iNOS, and eNOS to inflammation and carcinogenesis.
- To explore experimental evidence for these connections.
- To identify potential targets for cancer prevention and treatment.
Main Methods:
- Review of recent literature.
- Analysis of experimental evidence.
- Focus on NO/iNOS/eNOS modulation of cancer-related events.
Main Results:
- NO, iNOS, and eNOS modulate critical cancer events.
- These events include nitro-oxidative stress, apoptosis, cell cycle, angiogenesis, invasion, and metastasis.
- Experimental data support the role of NO signaling in cancer progression.
Conclusions:
- NO/iNOS/eNOS signaling is integral to inflammation and carcinogenesis.
- Targeting NO pathways presents opportunities for cancer prevention.
- Modulating NO production could be a strategy for cancer treatment.
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