The elucidation of the mechanisms controlling the metastatic processes is important for the development of new treatment methods to prevent the progression of localized disease to metastasis. Forkhead box D1 (FOXD1) is a member of the FOX transcription factor family and has been reported to play an important role in the devel-opment and progression of various cancers. However, its role in prostate cancer (PCa) remains only partially understood. Therefore, we aimed to explore the effects on the associated regulatory signal pathway of FOXD1 in prostate cancer. To clarify the roles of FOXD1 in prostate cancer, we used siRNA to suppress its expression in 22Rv1 cells with relatively higher expression of FOXD1. The effects of FOXD1 silencing on cell proliferation, migration and invasion were determined. WST-1 assays were used to determine cell proliferation. Cell migration and invasion were evaluated through wound healing and transwell assays. The possible underlying mechanism of FOXD1 silencing on 22Rv1 was evaluated by determining the expression of proteins related to EMT and Wnt/beta-catenin signaling pathway. Our results showed that FOXD1 was highly expressed in prostate cancer cell lines-PC-3, DU145, LNCaP and 22Rv1-compared to normal prostate epithelial cell line RWPE-1. Additionally, silencing of FOXD1 significantly reduced proliferation, migration and invasion of 22Rv1 cells. Furthermore, silencing of FOXD1 decreased the expression of beta-catenin and cyclin D1, which are involved in the Wnt/beta-catenin signaling pathway. However, it did not appear to affect the expression of EMT-related proteins other than N-cadherin. Our results suggest that silencing of FOXD1 suppresses metastatic potentials of the PCa via N-cadherin - Wnt/beta-catenin crosstalk. Therefore, the expression status of FOXD1 may be a new prognostic factor as well as a potential therapeutic target in prostate cancer treatment.