Open AccessFunction of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)
Author(s) -
Ruyi Li,
Rui Zhou,
Jiange Zhang
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.8355
Subject(s) - pathogenesis , lung cancer , cancer , immunology , copd , medicine , epigenetics , molecular medicine , cancer research , oncogene , inflammation , lung , oxidative stress , dna methylation , biology , cell cycle , pathology , biochemistry , gene expression , gene
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.