FOXK1 promotes cell growth through activating wnt/β-catenin pathway and emerges as a novel target of miR-137 in glioma.

Glioma is the most common primary malignant brain tumor in adults. Forkhead box k1 (FOXK1) was reported to be dysregulated and play important roles in multiple human cancers. However, the expression pattern and roles of FOXK1 in glioma has never been investigated. In this study, we firstly observed that the expression of FOXK1 was significantly increased in glioma tissue samples and cell lines. Functional assays demonstrated that overexpression of FOXK1 promoted proliferation, cell cycle transition and inhibited apoptosis in glioma cell lines. On the contrary, knockdown of FOXK1 exhibited an opposite effect on glioma cells proliferation, cell cycle and apoptosis. Data of western blot indicated that FOXK1 overexpression increased while FOXK1 knockdown decreased the levels of β-catenin, c-myc and cyclinD1 in glioma cells. Moreover, we demonstrated that FOXK1 was a novel target of miR-137 in glioma and FOXK1 restoration abolished the tumor suppressive effect of miR-137 in glioma cells. Statistical analysis showed that the mRNA level of FOXK1 was inversely correlated with miR-137 expression in glioma tissues. In conclusion, the present study demonstrated that FOXK1 promoted cell growth through activating wnt/β-catenin pathway and is negatively regulated by miR-137 in glioma.