Objective: To understand the role of WFDC2  in metastasis of ovarian cancer.
Methods: By knockdown or overexpression of WFDC2 , we demonstrated the role of WFDC2  in epithelial–mesenchymal transition (EMT).
Results: We demonstrated that stable knockdown of WFDC2  suppressed EMT along with the upregulation of E-cadherin and the downregulation of Vimentin. In addition, WFDC2  knockdown decreases matrix metalloproteinase-2 (MMP-2) expression in in vitro cell model and in in vivo nude mice xenografts. The correlation of WFDC2  and MMP-2 expression in the clinical sample confirmed that WFDC2  was tightly correlated with the development of tumor. More importantly, the EMT phenotype and cell invasion induced by WFDC2  overexpressing can be reversed by the siMMP-2 and P13K/AKT signaling inhibitor.
Conclusion: WFDC2  contributed to ovarian cancer metastasis and EMT as a positive regulator by activating AKT signaling pathway and inducing MMP-2 expression.
Keywords: WFCD2, ovarian cancer, metastasis, cell migration and invasion, epithelial-mesenchymal transition