Abstract
Ambient fine particulate matter (PM2.5) is one of the main environmental air pollutants that is closely related to the development of lung cancer, but the mechanisms are unclear. In this study, A549 cells were exposed to ambient PM2.5 to investigate the alterations of biological behaviors, and the possible role of miR-582-3p in the effects was further explored. The findings showed that PM2.5 exposure could significantly enhance the biological behaviors of A549 cells, and promote their epithelial-mesenchymal transition (EMT) transformation, especially at relatively low doses. Over-activation of Wnt/β-catenin signaling pathway and increased expression of miR-582-3p were also found in A549 cells after PM2.5 exposure. After the knockdown of miR-582-3p in A549 cells, the effects of PM2.5 on malignant biological behavior changes, EMT, and the activation of Wnt/β-catenin signaling pathway were all significantly alleviated. Furthermore, the inhibition of Wnt/β-catenin signaling pathway also inhibited the EMT process of A549 cells, which was rescued by the overexpression of miR-582-3p. Therefore, this study showed that ambient PM2.5 can upregulate the expression of miR-582-3p, consequently activate the Wnt/β-catenin signaling pathway, and thereby enhance EMT transformation and promote the malignant biological behaviors of A549 cells. These findings provide evidence for further research into the mechanisms by which exposure to PM2.5 in the environment promotes lung cancer.
Highlights
Air pollution is a major environmental issue that has substantial impacts on human health throughout the world[1]
A549 cells were exposed to ambient PM2.5 to investigate the alterations of biological behaviors, and the possible role of miR-582-3p in the effects was further explored
The findings showed that that PM2.5 exposure could significantly enhance the biological behaviors of A549 cells, and promote their epithelial-mesenchymal transition (EMT) transformation, especially at relatively low doses
Summary
Air pollution is a major environmental issue that has substantial impacts on human health throughout the world[1]. Due to the small particle size, light weight and high dispersion, PM2.5 can suspend in the air for long time and enter the alveoli through the respiratory tract. Part of the particulate matters can pass through the alveolar epithelium and enter the blood circulation through the lung tissue gap[2]. The International Agency for Research on Cancer (IARC) has classified particulate matter in ambient air as a Class I carcinogen[3]. Ambient fine particulate matter (PM2.5) is one of the main environmental air pollutants that closely related to the development of lung cancer, but the mechanisms are unclear
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