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.
Keywords: EMT; NNK; Peroxiredoxin I; lung cancer; oxidative damage.
Copyright: © Sun et al.