SB431542 inhibited cigarette smoke extract induced invasiveness of A549 cells via the TGF-β1/Smad2/MMP3 pathway.

Lung cancer has high morbidity and mortality rates. Smoking is involved in the pathogenesis of lung cancer, and tobacco smoke may increase tumor cell invasion and metastasis. The effects of cigarette smoke extract (CSE) on the carcinoma human alveolar basal epithelial A549 cell line were investigated. A549 cells were exposed to increasing concentrations of CSE for 12, 24 and 48 h, and the transforming growth factor-β1 (TGF-β1) signal pathway was inhibited by addition of SB431542, a TGF-β1 receptor antagonist. The proliferation of A549 cells was assayed by a Cell Counting kit-8, invasiveness was assayed using Transwell chambers, and TGF-β1, phosphorylated mothers against decapentaplegic homolog 2 (p-Smad2), and matrix metalloproteinase 3 (MMP3) levels was assessed by western blot analysis. The invasiveness of A549 cells and the expression of TGF-β1, pSmad2, and MMP-3 were significantly increased by CSE (P<0.05). The effects of CSE were abrogated by SB431542 (P<0.05). In conclusion, CSE increased the invasiveness of A549 cells and its effects were abrogated by SB431542 and the TGF-β1/Smad2/MMP-3 pathway may have been involved.