Salvianolic acid B acts against non‑small cell lung cancer A549 cells via inactivation of the MAPK and Smad2/3 signaling pathways
Guanglei Han, Yongzhong Wang, Tong Liu, Jiarong Gao, Fengyi Duan, Ming Chen, Yan Yang, Chao Wu
Abstract
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-/MaPK/Smad signaling axis was explored. a549 cells were co-cultured with and without different concentrations of Sal B (25, 50 and 100 M respectively) and TGF- 1 (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- 1 -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- 1 -stimulated a549 cells. overall, these results demonstrated that Sal B may have a potential therapeutic effect against nSclc in vitro. 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.