Abstract
Asiatic acid (AA) is a pentacyclic triterpenoid isolated from Centella asiatica (L.) Urban that possesses significant antitumor activities. In the present study, the mechanism of AA on transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) was investigated in the lung cancer cell line A549. To do so, cell morphological alterations were observed and recorded at different time periods. Cells treated with TGF-β1 were spindle-shaped and characterized as stromal cells, whereas AA-treated cells exhibited epithelial cell characteristics and increased intercellular adhesion. The MTT assay demonstrated that the high concentration of AA inhibited the viability of A549 cells treated with TGF-β. In addition, the wound healing and Transwell assays revealed that AA inhibited TGF-β1-induced invasion and migration of A549 cells. Furthermore, AA treatment increased the mRNA and protein expression levels of E-cadherin, and decreased the expression levels of snail family transcriptional repressor (Snail), N-cadherin, vimentin and β-catenin in TGF-β1-treated A549 cells. In conclusion, these results suggested that AA may inhibit TGF-β1-induced EMT in lung cancer through increased expression of E-cadherin, and inhibition of Snail, N-cadherin and vimentin expression.