Regulatory function of peroxiredoxin I on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung cancer development

Smoking is a major cause of lung cancer, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most important carcinogens in cigarette smoke. NNK modulates the expression of peroxiredoxin (Prdx) I in lung cancer. Prdx1 is upregulated in lung squamous cell carcinoma and lung adenocar...

Full description

Saved in:
Bibliographic Details
Published inOncology letters Vol. 21; no. 6; p. 465
Main Authors Sun, Hu-Nan, Ren, Chen-Xi, Gong, Yi-Xi, Xie, Dan-Ping, Kwon, Taeho
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.06.2021
Spandidos Publications UK Ltd
D.A. Spandidos
Subjects
Antioxidants
Apoptosis
Cancer
Carbon
Carcinogens
Cell growth
Cigarettes
Cytokines
Development and progression
DNA damage
Gene expression
Health aspects
Killer cells
Lung cancer
Metabolism
Metabolites
Mutation
Nitrogen
Oncology
Oncology, Experimental
Oxidative stress
Peptides
Proteins
Review
Smoking
Squamous cell carcinoma
Tobacco
Tumors
lung cancer
oxidative damage
NNK
EMT
Peroxiredoxin I
Online AccessGet full text

Cover

More Information
Summary:Smoking is a major cause of lung cancer, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most important carcinogens in cigarette smoke. NNK modulates the expression of peroxiredoxin (Prdx) I in lung cancer. Prdx1 is upregulated in lung squamous cell carcinoma and lung adenocarcinoma, and considered a potential biomarker for lung cancer. The current article reviewed the role and regulatory mechanisms of Prdx1 in NNK-induced lung cancer cells. Prdx1 protects erythrocytes and DNA from NNK-induced oxidative damage, prevents malignant transformation of cells and promotes cytotoxicity of natural killer cells, hence suppressing tumor formation. In addition, Prdx1 has the ability to prevent NNK-induced lung tumor metabolic activity and generation of large amount of reactive oxygen species (ROS) and ROS-induced apoptosis, thus promoting tumor cell survival. In contrast to this, Prdx1, together with NNK, can promote the epithelial-mesenchymal transition and migration of lung tumor cells. The signaling pathways associated with NNK and Prdx1 in lung cancer cells have been discussed in present review; however, numerous potential pathways are yet to be studied. To develop novel methods for treating NNK-induced lung cancer, and improve the survival rate of patients with lung cancer, further research is needed to understand the complete mechanism associated with NNK.
Bibliography:Contributed equally
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2021.12726