Objective To study the effects of nicotine on cell proliferation,invasion and migration of A549 and explore the possible mechanisms.Methods The abilities of proliferation,migration and invasion of A549 cell were measured by CCK-8,Transwell test,and wound scratch assay respectively.The expressions ofα7 nicotinic acetylcholine receptor (nAChR),vascular endothelial growth factor (VEGF) and matrix metalloproteinase-2 (MMP-2) were observed by Western blot.Results Compared with the control group,10-6 mol/L nicotine promoted A549 proliferation,migration and invasion significantly (all P <0.05).Nicotine increased the protein expressions ofα7 nAChR,VEGF and MMP-2.Conclusions Nicotine can increase proliferation,migration and invasion of human lung adenocarcinoma A549 cell throughα7 nAChR,which may be associated with the upregulation of VEGF and MMP-2 protein expressions.

Objective: To observe if arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5(WSPM2.5) exposure can induce epithelial-mesenchymal transition (EMT) in human bronchial cells (HBEC). Methods: PM2.5 was collected from an arterial traffic road and a typical southern kitchen, and then the collections were extracted by DMSO. The viability of HBEC was measured by Cell Counting Kit (CCK-8) after culture with PM2.5-DMSO extracts for 24 hours. The expressions of EMT markers, including E-cadherin, cytokeratin, α-smooth muscle actin (α-SMA), vimentin and collagen typeⅠ (COL-Ⅰ) in HBEC were assayed by cell immunofluorescence and Western blot analysis after exposed to two different sources of PM2.5-DMSO extracts for 14 days. Results: The cell viability of HBEC increased at low concentrations (1, 2, 10 μg/ml and 1, 5, 10 μg/ml, corresponding to [(118.4±13.7)%, (118.2±8.0)%, (123.0±19.6)% and (112.4±4.1)%, (120±5.4)%, (117.8±7.0)%, respectively, all P<0.05], and then declined at high levels [20, 100, 200 μg/ml and 15, 20, 30, 40 μg/ml, corresponding to (100.7±12.1)%, (53.4±15.3)%, (9.4±1.7)% and (106.8±10.0)%, (93.8±7.9)%, (60.9±9.5)%, (46.2±3.6)%, respectively, P values were 0.923, 0.000, 0.000 and 0.231, 0.278, 0.000, 0.000, respectively] in both TAPM2.5-DMSO and WSPM2.5-DMSO incubation. After exposure for 14 days, the cells lost their typical cobblestone-like shape which implied that EMT might occur. The same treatment caused decreased positive signals of E-cadherin and cytokeratin in a small proportion of the cells. The decreased expressions of cytokeratin were verified by Western blot (TAPM2.5 and WSPM2.5 were 0.063±0.109 and 0.039±0.313, P values were 0.033 and 0.030, respectively), while α-SMA was only significantly upregulated in the WSPM2.5-DMSO group (7.853±4.784, P=0.049). The expressions of E-cadherin decreased in both groups but not statistically significant in Western blot (0.862±0.096 and 0.817±0.212, P values were 0.228 and 0.117, respectively). Another marker of EMT, COL-I, markedly increased in both PM2.5 treatment groups (2.549±1.037 and 3.658±1.207, P values were 0.034 and 0.001). Conclusions: Both PM2.5 from arterial traffic ambient air and wood smoke could induce EMT in human bronchial epithelial cells, while WSPM2.5 appeared to have a more significant influence on EMT in HBEC.