Nicotine Induced Lung Cancer Cells Epithelial-mesenchymal Transition 
and Promote Its Vitro Invasion Potential

• Published in: Zhongguo fei ai za zhi 2016-04, Vol.19 (4), p.169-176
• Main Authors: Hou, Yanxu, Li, Xuebing, Pan, Zhenhua, Zu, Lingling, Fan, Yaguang, You, Jiacong, Wang, Yuli, Wang, Min, Chen, Peirui, Shen, Wang, Zhou, Qinghua
• Format: Article
• Language: Chinese
• Subjects: A549 Cells; Angiogenesis; beta Catenin - genetics; beta Catenin - metabolism; Breast cancer; Cadherins - genetics; Cadherins - metabolism; Cell Movement - drug effects; Epithelial-mesenchymal transition; Epithelial-Mesenchymal Transition - drug effects; Gene Expression Regulation, Neoplastic; Humans; Invasion; Lung cancer; Lung neoplasms; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - physiopathology; Medical screening; Metastasis; Neoplasm Invasiveness; Nicotine; Nicotine - adverse effects; Proteins; Tobacco smoke; Vimentin - genetics; Vimentin - metabolism
• ISSN: 1009-3419; 1999-6187
• DOI: 10.3779/j.issn.1009-3419.2016.04.11

Our previous study found that nicotine could induce lung cancer cell epithelial-mesenchymal transition (EMT). The aim of this study is to explore the relationship between nicotine-induced EMT and lung cancer invasion and metastasis. Real-time PCR and Western blot were used to detect the expression changes of EMT-related markers, E-cadherin and Vimentin, in A549 lung cancer cells treated with nicotine; The transposition of β-catenin protein expression was determined by immunofluorescence; Scratch test and Transwell invasion assay were used to detect the effects of nicotine on lung cancer cell migration and invasion. Nicotine can significantly down-regulate the expressional level of E-cadherin mRNA and protein of A549 cells in a manner of dose and time-dependent (P