Forkhead Box K1 Expression Research Articles

FOXK1 plays an oncogenic role in the development of esophageal cancer

Forkhead box k1 (FOXK1) is a member of the FOX class of transcription factors and it is dysregulated in many solid tumors including hepatocellular carcinoma, gastric cancer, colorectal cancer and prostate cancer. However, the expression status of FOXK1 and its clinical significance in esophageal cancer (EC) is still uncertain. Our study aimed at investigating the significance of FOXK1 expression in human EC and its biological function in the development of EC. We found that FOXK1 was overexpressed in EC tissues compared with corresponding non-tumor tissues using immunohistochemistry. And high FOXK1 expression was related to poor differentiation of EC. The Kaplan-Meier curve indicated that high FOXK1 expression may result in poor prognosis of EC patients. Furthermore, overexpression of FOXK1 in EC9706 cell inhibited cell apoptosis and promoted cell proliferation and migration, and suppression of FOXK1 in EC109 cell obtained reverse results. Our data suggest that FOXK1 plays an oncogenic role in EC pathogenesis and can serve as a therapeutic target for patients with EC.

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

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.

Knockdown of FOXK1 inhibited the proliferation, migration and invasion in hepatocellular carcinoma cells

FOXK1 (forkhead box k1), a member of the FOX family, is overexpressed in several types of solid tumors. However, the biological function of FOXK1 in hepatocellular carcinoma (HCC) remains poorly understood. In the present study, we investigated the expression status and functional roles of FOXK1 in HCC. Our results demonstrated that the expression of FOXK1 was significantly up-regulated in human HCC tissues and cell lines. In addition, down-regulation of FOXK1 suppressed the proliferation, migration and invasion of HCC cells in vitro, as well as attenuated tumor growth in nude mice model. We further elucidated that knockdown of FOXK1 down-regulated the protein expression levels of β-catenin, c-myc and cyclin D1 in HepG2 cells. In conclusion, the present study indicated that FOXK1 may act as an oncogene in human HCC, and knockdown of FOXK1 significantly inhibited HCC cell proliferation, migration and invasion, partly through the inactivation of Wnt/β-catenin signaling pathway. These findings suggest that FOXK1 may be a novel therapeutic target to treat HCC.