1.Nicotine Induced Lung Cancer Cells Epithelial-mesenchymal Transition and Promote Its Vitro Invasion Potential
HOU YANXU ; LI XUEBING ; PAN ZHENHUA ; ZU LINGLING ; FAN YAGUANG ; YOU JIACONG ; WANG YULI ; WANG MIN ; CHEN PEIRUI ; SHEN WANG ; ZHOU QINGHUA
Chinese Journal of Lung Cancer 2016;19(4):169-176
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;hTe transposition ofβ-catenin protein expression was determined by immunolfuorescence;Scratch test and Transwell invasion assay were used to detect the effects of nicotine on lung cancer cell migration and invasion. Results Nicotine can signiifcantly 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 signiifcantly 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);Immunolfuorescence results showed thatβ-catenin protein was signiifcantly transfered to nucleus;Scratch test and Transwell assay showed that Nicotine could remarkably increase the migration and invasion poten-tial 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.
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