• Breast cancer;
  • epithelial-mesenchymal transition;
  • glabridin;
  • metastasis;
  • microRNA-200c

Current treatments for breast cancer, a common malignancy in human females, are less than satisfactory because of high rates of metastasis. Glabridin (GLA), which acts through the FAK/ROS signaling pathway, has been used as an antioxidant and anti-metastatic agent. However, little is known regarding the effect of microRNA (miRNA) on GLA's anti-metastatic activity. The miRNA-200 family, which is frequently expressed at low levels in triple negative breast cancers, inhibits metastasis by blocking the epithelial–mesenchymal transition. Here, we found that GLA attenuated the migratory and invasive capacity of breast cancer cells by activating miR-200c. GLA induced the mesenchymal–epithelial transition in vitro and in vivo, as determined by increased expression of the epithelial marker, E-cadherin, and decreased expression of the mesenchymal marker, vimentin. Overexpression of miR-200c enhanced the expression of E-cadherin and decreased the expression of vimentin. Furthermore, in MDA-MB-231 and BT-549 breast cancer cells exposed to GLA, knockdown of miR-200c blocked the GLA-induced mesenchymal–epithelial transition and alleviated the GLA-induced inhibition of migration and invasion. Thus, elevation of miR-200c by GLA has considerable therapeutic potential for anti-metastatic therapy for breast cancer patients.