Exosomes from PM^(2.5)-treated Human Bronchial Epithelial Cells Increase Lung Cancer Metastatic Potential

作     者：YU Heng Yi GUO Hua Qi FENG Yan CHENG Wei WANG Yan YU Heng Yi;GUO Hua Qi;FENG Yan;CHENG Wei;WANG Yan

作者机构：School of Public HealthShanghai Jiao Tong University School of MedicineShanghai 200025China The Ninth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200011China 

出 版 物：《Biomedical and Environmental Sciences》 (生物医学与环境科学（英文版）)

年 卷 期：2022年第35卷第6期

页      面：473-484页

核心收录：

学科分类：0830[工学-环境科学与工程（可授工学、理学、农学学位）] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：supported by the Natural Science Foundations of China 

主　　题：Fine particulate matter Exosome Lung cancer C-Jun N-terminal kinase Bronchial epithelial cell 

摘      要：Objective Fine particulate matter(PM^(2.5))is an air pollutant that has become of great concern in recent years.Numerous studies have found that PM^(2.5)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 PM^(2.5)-promoted lung cancer metastasis.Methods Exosomes 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 PM^(2.5)-treated human bronchial epithelial cells(PHBE-exo).Results The 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 Nterminal kinase.Conclusion These results implied that PM^(2.5)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.