In addition, the inactivating mutation FBXO11 S187A failed to promote the acquisition of various phenotypes characteristic of the EMT in prostate cancer; for example, compared to FBXO11 overexpression, it induced scratch wound closure (Fig. 3N), cell migration (Fig. 3O), E-cadherin membrane disruption and endocytosis (Fig. 3P), and pseudopodia formation (Fig. 3Q). This evidence concerns the gene FBXO11 and prostate cancer.