Cortactin is involved in transforming growth factor-beta1-induced epithelial-mesenchymal transition in AML-12 cells.

Cortactin is an F-actin binding protein, regulating cell movement and adhesive junction assembly. However, the function of cortactin in epithelial-mesenchymal transition (EMT) remains elusive. Here we found that during transforming growth factor-beta1 (TGF-beta1)- induced EMT in AML-12 murine hepatocytes, cortactin underwent tyrosine dephosphorylation. Inhibition of the dephosphorylation of cortactin by sodium vanadate blocked TGF-beta1-induced EMT. Knockdown of cortactin by RNAi led to decrease of intercellular junction proteins E-cadherin and Zonula occludens-1 and induced expression of mesenchymal protein fibronectin. Additionally, knockdown of cortactin further promoted TGF-beta1-induced EMT in AML-12 cells, as determined by EMT markers and cell morphological changes. Moreover, migration assay showed that cortactin knockdown promoted the migration of AML-12 cells, and also enhanced TGF-beta1-induced migration. Our study showed the involvement of cortactin in the TGFbeta1- induced EMT.