Abstract
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.
DOI
10.2147/cmar.s192950
Publication Date
2019-03-27
Publication Title
Cancer Management and Research
Volume
Volume 11
Publisher
Dove Medical Press
ISSN
1179-1322
Embargo Period
2024-11-19
First Page
2415
Last Page
2424
Recommended Citation
Chen, Y., Huang, L., Wang, S., Li, J., & et al. (2019) 'WFDC2 contributes to epithelial-mesenchymal transition (EMT) by activating AKT signaling pathway and regulating MMP-2 expression', Cancer Management and Research, Volume 11, pp. 2415-2424. Dove Medical Press: Available at: https://doi.org/10.2147/cmar.s192950
