Together, these results suggest that KuA inhibited human GBM cell growth through apoptosis induction by decreasing the expressions of 5-Lipoxygenase and Bcl-2, increasing expressions of Bax and active caspaes-3; it suppressed GBM cell migration through epithelial-mesenchymal transition attenuation by downregulating the expressions of C/EBPβ, N-cadherin, vimentin, twist and snail+slug, and upregulating the expression of E-cadherin. Here, BAX is linked to glioblastoma.