Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

  • Authors:
    • Ruyi Li
    • Rui Zhou
    • Jiange Zhang
  • View Affiliations

  • Published online on: March 26, 2018     https://doi.org/10.3892/ol.2018.8355
  • Pages: 7506-7514
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Abstract

Previous research has identified that air pollution is associated with various respiratory diseases, but few studies have investigated the function served by particulate matter 2.5 (PM2.5) in these diseases. PM2.5 is known to cause epigenetic and microenvironmental alterations in lung cancer, including tumor‑associated signaling pathway activation mediated by microRNA dysregulation, DNA methylation, and increased levels of cytokines and inflammatory cells. Autophagy and apoptosis of tumor cells may also be detected in lung cancer associated with PM2.5 exposure. A number of mechanisms are involved in triggering and aggravating asthma and COPD, including PM2.5‑induced cytokine release and oxidative stress. The present review is an overview of the underlying molecular mechanisms of PM2.5‑induced pathogenesis in lung cancer and chronic airway inflammatory diseases.
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May-2018
Volume 15 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Li R, Zhou R and Zhang J: Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review). Oncol Lett 15: 7506-7514, 2018.
APA
Li, R., Zhou, R., & Zhang, J. (2018). Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review). Oncology Letters, 15, 7506-7514. https://doi.org/10.3892/ol.2018.8355
MLA
Li, R., Zhou, R., Zhang, J."Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)". Oncology Letters 15.5 (2018): 7506-7514.
Chicago
Li, R., Zhou, R., Zhang, J."Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)". Oncology Letters 15, no. 5 (2018): 7506-7514. https://doi.org/10.3892/ol.2018.8355