Exosomes from PM2.5-treated Human Bronchial Epithelial Cells Increase Lung Cancer Metastatic Potential

Abstract

ObjectiveFine particulate matter (PM2.5) is an air pollutant that has become of great concern in recent years. Numerous studies have found that PM2.5 may contribute to lung cancer, but the pathogenesis has not yet been fully elucidated. In this study, we explored the roles of exosomes from bronchial epithelial cells in PM2.5-promoted lung cancer metastasis. MethodsExosomes were isolated from cell supernatants. An animal model of lung metastasis (established by tail vein injection of A549-luc) and in vitro studies with lung cancer cell lines were used to investigate the effects of exosomes derived from PM2.5-treated human bronchial epithelial cells (PHBE-exo). ResultsThe animal experiments revealed that PHBE-exo-treated mice showed stronger luciferase activity and a larger relative metastatic region in the lungs, thus indicating that PHBE-exo promoted the metastatic potential of lung cancer. Additionally, PHBE-exo promoted the migration, invasion and epithelial-to-mesenchymal transition of lung cancer cells, in a manner mediated by activation of c-Jun N-terminal kinase. ConclusionThese results implied that PM2.5 may promote the development of lung cancer through exosomes derived from bronchial epithelial cells, thus providing a potential interventional target for lung cancer. These findings broadened our understanding of cancer-promoting mechanisms of environmental pollutants.