FOXC1 silencing inhibits the epithelial-to-mesenchymal transition of glioma cells: Involvement of β-catenin signaling

Glioma is a type of malignant brain tumor. Forkhead box C1 (FOXC1) is a conserved transcription factor that is involved in tumorigenesis; however, the function of FOXC1 in glioma remains unclear. The present study aimed to investigate the effects of FOXC1 silencing on the epithelial-to-mesenchymal transition (EMT) of glioma cells. FOXC1-specific small interfering RNAs were employed to downregulate the expression levels of FOXC1 in glioma cells. The proliferation, migration and invasion of glioma cells were assessed by MTT assay, wound healing assay and Transwell assay. Western blot analysis was performed to reveal the effects of FOXC1 on EMT-associated proteins and β-catenin signaling. The results revealed that, following FOXC1 silencing, the proliferation, migration and invasion of glioma cells were decreased. The expression levels of EMT-associated proteins were also affected. Further examination demonstrated that β-catenin signaling was involved in the effects of FOXC1 on glioma cells. Previous results suggested that overexpression of β-catenin reversed the effects of FOXC1 silencing on glioma cells. The present study demonstrated that FOXC1 may regulate the EMT of glioma cells, potentially via β-catenin signaling. Therefore, FOXC1 may be a potential therapeutic target for the treatment of glioma.