Forkhead box K1 (FOXK1) is a member of the FOX
transcription factor family and plays an important role in the development of several
tumors. However, the role of FOXK1 in the progression of
prostate cancer remains unknown. Thus, the objectives of this study were to detect the expression of FOXK1 in
prostate cancer and to examine its role in
prostate cancer cells. We found that the expression of FOXK1 at both the
mRNA and
protein levels was significantly upregulated in human
prostate cancer cell lines. In addition, the downregulation of FOXK1 obviously inhibited the cell proliferation of
prostate cancer cells in vitro and attenuated
tumor growth in a xenograft model in vivo. Furthermore, knockdown of FOXK1 suppressed the migration and invasion of
prostate cancer cells, and prevented the EMT phenotype through upregulating the expression of
E-cadherin, as well as downregulating the expression of
N-cadherin in
prostate cancer cells. Mechanistically, knockdown of FOXK1 efficiently downregulated the expression levels of β-
catenin, c-myc, and
cyclin D1 in PC-3 cells. Overall, our results demonstrated that knockdown of FOXK1 inhibited the proliferation and
metastasis of
prostate cancer, at least in part, through suppressing the Wnt/β-
catenin signaling pathway. Therefore, these results suggest that FOXK1 may be a potential therapeutic target for human
prostate cancer.