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Background  The adhesion molecule, FAT4, has a tumor suppressor function with a critical role in the epithelial-to-mesenchymal-transition (EMT) and anti-malignant growth in several cancers. No study has investigated yet its role in epithelial ovarian cancer (EOC) progression. In the present study, we examined the role of  FAT4  in proliferation and metastasis, and its mechanisms of interaction in these processes.    Methods  We have performed cell viability, colony formation, and invasion assays in ovarian cancer cells treated with siRNA to knockdown  FAT4  gene expression. The regulatory effects of FAT4 on proteins involved in apoptotic, Wnt, Hippo, and retinoblastoma signaling pathways were evaluated by Western blotting following FAT4 repression. Also, 426 ovarian tumor samples and 88 non-tumor samples from the Gene Expression Profiling Interactive Analysis (GEPIA) database were analyzed for the expression of  FAT4 . Pearson’s correlation was performed to determine the correlation between  FAT4  and the  E2F5 ,  cyclin D1 ,  cdk4 , and  caspase 9  expressions.    Results  Lower expression of FAT4 was observed in ovarian cancer cell lines and human samples as compared to non-malignant tissues. This down-regulation seems to enhance cell viability, invasion, and colony formation. Silencing  FAT4  resulted in the upregulation of  E2F5 , vimentin, YAP, β-catenin, cyclin D1, cdk4, and Bcl2, and in the downregulation of GSK-3-β, and caspase 9 when compared to control. Furthermore, regulatory effects of FAT4 on the EMT and aggressive phenotype seem to occur through Hippo, Wnt, and cell cycle pathways.    Conclusion   FAT4  downregulation promotes increased growth and invasion through the activation of Hippo and Wnt-β-catenin pathways.

FAT4 silencing promotes epithelial-to-mesenchymal transition and invasion via regulation of YAP and β-catenin activity in ovarian cancer