尼古丁诱导肺癌细胞上皮间质转化促进其侵袭转移

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.