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

• Main Authors: Yanxu HOU, Xuebing LI, Zhenhua PAN, Lingling ZU, Yaguang FAN, Jiacong YOU, Yuli WANG, Min WANG, Peirui CHEN, Wang SHEN, Qinghua ZHOU
• Format: Article
• Language: zho
• Published: Chinese Anti-Cancer Association; Chinese Antituberculosis Association 2016-04-01
• Series: Chinese Journal of Lung Cancer
• Subjects: Lung neoplasms; Nicotine; Epithelial-mesenchymal transition; Invasion
• Online Access: http://dx.doi.org/10.3779/j.issn.1009-3419.2016.04.11

Background and objective 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. Methods 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. Results 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<0.01, P<0.01); Nicotine can significantly up-regulate the expressional level of Vimentin mRNA and protein of A549 cells in a manner of dose and time-dependent (P<0.01, P<0.01); Immunofluorescence results showed that β-catenin protein was significantly transfered to nucleus; Scratch test and Transwell assay showed that Nicotine could remarkably increase the migration and invasion potential of lung cancer cells (P<0.01, P<0.01). Conclusion Nicotine can induce cancer cells EMT, and promote the invasion and metastasis ability of lung cancer cells.