Knockdown of FOXK1 Suppresses Proliferation, Migration, and Invasion in Prostate Cancer Cells

摘要

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