To verify whether CAV-1 activated PI3K/Akt signaling in glioma cells through regulation of PAI-1, we detected the levels of PI3K and Akt in PAI-1-silenced cells with CAV-1 over-expression and observed that PAI-1 knockdown decreased the expression of p-PI3K, p-Akt, Vimentin and N-cadherin, and the expression of these proteins were not reversed following the over-expression of CAV-1 (Fig. 5A and B). Here, AKT1 is linked to central nervous system cancer.