Salvianolic acid B acts against non‑small cell lung cancer A549 cells via inactivation of the MAPK and Smad2/3 signaling pathways.

Salvianolic acid B (Sal B) is a potential cytotoxic polyphenol against cancer. In the present study the effect of Sal B and its molecular mechanism were investigated in the non‑small cell lung cancer (NSCLC) A549 cell line. The TGF‑β/MAPK/Smad signaling axis was explored. A549 cells were co‑cultured with and without different concentrations of Sal B (25, 50 and 100 µM respectively) and TGF‑β1 (9 pM) for 24 h. Cell epithelial‑mesenchymal transition (EMT), cell migration, cell cycle distribution, autophagy and apoptosis were assessed by western blotting (WB), wound healing assay and flow cytometry, respectively. Moreover, activation of MAPK, Smad2/3 and the downstream target, plasminogen activator inhibitor 1 (PAI‑1), were assessed by WB. The results demonstrated that Sal B inhibited TGF‑β1‑induced EMT and migration of A549 cells, hampered cell cycle progression and induced cell autophagy and apoptosis. Furthermore, Sal B inactivated MAPK signaling pathways and the phosphorylation of Smad2/3, especially the phosphorylation of Smad3 at the linker region, which resulted in decreased protein expression levels of PAI‑1 in TGF‑β1‑stimulated A549 cells. Overall, these results demonstrated that Sal B may have a potential therapeutic effect against NSCLC . The results of the present study indicated that the underlying active mechanism of Sal B in NSCLC may be closely related to the impeded activation of the MAPK and Smad2/3 signaling pathways. Therefore, Sal B may be a potential candidate NSCLC therapeutic agent.