机构：[1]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China,[2]Cancer Epidemiology Program, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, USA
Background/Aims: Ecological studies have shown that air pollution and prevalence of cigarette smoking are positively correlated. Evidence also suggests a synergistic effect of cigarette smoking and PM2.5 exposure (Environmental Particulate Matter <= 2.5 mu m in diameter) on lung cancer risk. We aimed to evaluate the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality and determine its underlying mechanisms in vitro. Methods: "MOVER" method was used to analyze the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality. Cell autophagy and malignant behaviors induced by cigarette smoke extract (CSE) and PM2.5 exposure were examined in vitro. Gene expression was examined by qRT-PCR and western blot. RNA and protein interaction was determined using a RNA binding protein immunoprecipitation assay. Results: An increased risk for lung cancer death (RERI (the relative excess risk) =0.28) was observed with a synergistic interaction between cigarette smoking and PM2.5 pollution. Cell migration, invasion, EMT (epithelial-mesenchymal transition) and autophagy were elevated when lung cancer cells were treated with CSE and PM2.5 in combination. A lncRNA, named lung cancer progression-association transcript 1 (LCPAT1), was up-regulated after the treatment of CSE and PM2.5, and knocking down the lncRNA impaired the effect of CSE and PM2.5 on lung cancer cells. In addition, LCPAT1 was shown to bind to RCC2, and RCC2 mediated the effect of LCPAT1 on cell autophagy, migration, invasion and EMT in lung cancer. Conclusions: Our results suggest that combined exposure to CSE and PM2.5 induces LCPAT1 expression, which up-regulates autophagy, and promotes lung cancer progression via RCC2. (C) 2018 The Author(s) Published by S. Karger AG, Basel
基金：
National Natural Science Foundation of China (grant nos. 81573232, B.Q., 81602929, N.F.) and the Three-year Action Plan on Public Health, Phase Ⅳ, Shanghai, China (grant nos. 15GWZK0801).
第一作者机构：[1]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China,
共同第一作者：
通讯作者：
通讯机构：[1]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China,[*1]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital and Faculty of Public Health Shanghai Jiao Tong University School of Medicine, Shanghai (China)
推荐引用方式(GB/T 7714)：
Lin Hongyan,Zhang Xiaohong,Feng Nannan,et al.LncRNA LCPAT1 Mediates Smoking/Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2[J].CELLULAR PHYSIOLOGY AND BIOCHEMISTRY.2018,47(3):1244-1258.doi:10.1159/000490220.
APA：
Lin, Hongyan,Zhang, Xiaohong,Feng, Nannan,Wang, Ruoyang,Zhang, Weituo...&Qian, Biyun.(2018).LncRNA LCPAT1 Mediates Smoking/Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2.CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,47,(3)
MLA：
Lin, Hongyan,et al."LncRNA LCPAT1 Mediates Smoking/Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2".CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 47..3(2018):1244-1258
