Torilis japonica extract, a new potential EMT suppressor agent by regulation of EGFR signaling pathways

Abnormal metastasis of carcinoma is associated with the loss of epithelial features and the acquisition of a mesenchymal phenotype. The stimulation of cells with epidermal growth factor (EGF) resulted in morphological changes and induced epithelial-mesenchymal transition (EMT). EGF stimulation resulted in increased mobility along with upregulated actin polarization related proteins, E-cadherin regulators and the mesenchymal markers. Treatment with Torilis japonica extract (TJE) along with stimulation by EGF prevented changes in cell morphology, mobility, expression of actin polarization proteins and EMT markers. Using specific inhibitors and siEGFR, it was demonstrated that TJE suppressed EMT through EGFR inactivation and regulation of its downstream signaling pathways. We suggest that TJE is a new potential reagent for EGFR-targeted therapy and anti-abnormal metastasis in MCF-7 breast cancer.