Both ectopic LRRC4 overexpression, or the restoration of LRRC4 endogenous expression inhibited the expression of BRD7, locked-nucleic-acid (LNA)-mediated miR-182 and -381 silencing specifically targeted the LRRC4 and led to perturbations in the Ras/Raf/ERK/MAPK and PI-3K/AKT signaling pathways and to down-regulation of BRD7, which inhibited glioma growth. Here, AKT1 is linked to central nervous system cancer.