FOXC1 promotes proliferation and epithelial-mesenchymal transition in cervical carcinoma through the PI3K-AKT signal pathway.

Recently, Forkhead box C1 (FOXC1) has been identified to play important roles in human cancers. However, the clinical significance and biological role of FOXC1 in cervical cancer remains unclear. Here, we showed that FOXC1 was frequently overexpressed in cervical cancer versus adjacent non-tumor tissues. Overexpression of FOXC1 was significantly correlated with tumor stage (P=0.011), tumor size (P=0.034), stromal invasion (P= 0.001), and lymph nodes metastasis (P=0.008). Survival analysis further suggested that high FOXC1 expression was significantly correlated with poor overall survival (P=0.007) and recurrence-free survival (P=0.003) in cervical cancer patients. Moreover, we found that knock-down of FOXC1 by short hairpin RNAi significantly suppressed cervical cancer cells proliferation, migration, and invasion in vitro. Mechanistic studies showed that the FOXC1 requires PI3K/AKT signaling for its regulation of cell proliferation, migration and invasion. Our findings indicate that FOXC1 plays an important oncogenic role in cervical cancer progression.