Open Access

ARTICLE

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

by

* Organ Transplantation Center, Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital, Chengdu, P.R. China
† Department of Urology, Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital, Chengdu, P.R. China
‡ The East Ward, Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital, Chengdu, P.R. China
1 These authors provided equal contribution to this work.

Oncology Research 2017, 25(8), 1261-1267. https://doi.org/10.3727/096504017X14871164924588

Abstract

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.

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