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

  • Authors:
    • Hu-Nan Sun
    • Chen-Xi Ren
    • Yi-Xi Gong
    • Dan-Ping Xie
    • Taeho Kwon
  • View Affiliations / Copyright

    Affiliations: College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang 163319, P.R. China, Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup, Jeonbuk 56216, Republic of Korea
    Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 465
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    Published online on: April 12, 2021
       https://doi.org/10.3892/ol.2021.12726
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Sun H, Ren C, Gong Y, Xie D and Kwon T: Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review). Oncol Lett 21: 465, 2021.
APA
Sun, H., Ren, C., Gong, Y., Xie, D., & Kwon, T. (2021). Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review). Oncology Letters, 21, 465. https://doi.org/10.3892/ol.2021.12726
MLA
Sun, H., Ren, C., Gong, Y., Xie, D., Kwon, T."Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review)". Oncology Letters 21.6 (2021): 465.
Chicago
Sun, H., Ren, C., Gong, Y., Xie, D., Kwon, T."Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review)". Oncology Letters 21, no. 6 (2021): 465. https://doi.org/10.3892/ol.2021.12726
Copy and paste a formatted citation
x
Spandidos Publications style
Sun H, Ren C, Gong Y, Xie D and Kwon T: Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review). Oncol Lett 21: 465, 2021.
APA
Sun, H., Ren, C., Gong, Y., Xie, D., & Kwon, T. (2021). Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review). Oncology Letters, 21, 465. https://doi.org/10.3892/ol.2021.12726
MLA
Sun, H., Ren, C., Gong, Y., Xie, D., Kwon, T."Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review)". Oncology Letters 21.6 (2021): 465.
Chicago
Sun, H., Ren, C., Gong, Y., Xie, D., Kwon, T."Regulatory function of peroxiredoxin I on 4‑(methylnitrosamino)‑1‑(3‑pyridyl)‑1‑butanone‑induced lung cancer development (Review)". Oncology Letters 21, no. 6 (2021): 465. https://doi.org/10.3892/ol.2021.12726
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