%0 Journal Article
%T Nicotine Induced Lung Cancer Cells Epithelial-mesenchymal Transition £¿and Promote Its Vitro Invasion Potential
%A Yanxu HOU
%A Xuebing LI
%A Zhenhua PAN
%A Lingling ZU
%A Yaguang FAN
%A Jiacong YOU
%A Yuli WANG
%A Min WANG
%A Peirui CHEN
%A Wang SHEN
%A Qinghua ZHOU
%J Öйú·Î°©ÔÓÖ¾
%D 2016
%R : 10.3779/j.issn.1009-3419.2016.04.11
%X 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 ¦Â-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 ¦Â-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.
%K Lung neoplasms
%K Nicotine
%K Epithelial-mesenchymal transition
%K Invasion
%U http://www.lungca.org/index.php?journal=01&page=article&op=view&path%5B%5D=10.3779%2Fj.issn.1009-3419.2016.04.11