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Objective To investigate the effect and underlying mechanism of cigarette smoke extract (CSE) on invasion ability of lung adenocarcinoma PC-9 cells. Methods PC-9 cells were cultured in the medium containing 0%, 1%, 2% and 4% tobacco smoke extract for 96 h, respectively. The invasive ability of the cells was detected by Transwell assay. The protein levels of NLRP3, Caspase-1, IL-1β and MMP-2 were measured with Western blotting. After co-treatment with 4% CSE and NLRP3 inhibitor, MCC950, for 96 h, Transwell assay was employed again for the invasive ability of the cells, and Western blotting for the expression of NLRP3, Caspase-1, IL-1β and MMP-2. Results CSE significantly increased the invasive ability of PC-9 cells (P < 0.05, P < 0.01) and promoted the protein expression of NLRP3, Caspase-1, IL-1β and MMP-2(P < 0.01) in dose-dependent manners. The intervention of MCC950 obviously inhibited the enhanced invasive ability of PC-9 cells and the up-regulation of NLRP3, Caspase-1, IL-1β and MMP-2 induced by CSE. Conclusion CSE enhances the invasive ability of lung adenocarcinoma cells, which may be associated with the activation of NLRP3 inflammasome.