Abstract
Lung cancer begins in the lung and is a leading cause of premature death. Forkhead box C1 (FOXC1) has been reported to play an important role in different types of cancer, and evidence suggests that FOXC1 is highly expressed in non-small cell lung cancer (NSCLC) patients. However, the function and molecular mechanism of FOXC1 in the NSCLC cell line A549 is still unclear. In the present study, we indicate that FOXC1 is expressed in the NSCLC cell lines A549, H460, and SK-MES-1 at a high level compared with control human bronchial epithelial (HBE) cells. FOXC1 silencing promotes A549 cell apoptosis, whereas it inhibits cell survival. The levels of anti-apoptosis protein Bcl-2 decreased and the expression of pro-apoptosis protein Bax increased in FOXC1 silenced cells. Further studies show that FOXC1 knockdown inhibits the PI3K/AKT/hedgehog/Gli2 pathway. Overexpressed AKT or Gli2 reversed the effects of FOXC1 silencing on A549 cell survival and apoptosis. Taken together, our results conclude that FOXC1 silencing reduced the survival of cancer cells and promoted their apoptosis, and that the PI3K/AKT/hedgehog/Gli2 pathway plays an important role in the functioning of FOXC1 silencing.