<div><p>Inactivated <i>LRRC4</i> has been clinically detected in gliomas, and promoter hypermethylation has been implicated as the mechanism of inactivation in some of those tumors. Our previous researches indicated that <i>LRRC4</i> is a target gene of miR-381, the interaction of miR-381 and <i>LRRC4</i> is involved in glioma growth. In this study, we demonstrate that <i>LRRC4</i> is a target gene of the other microRNA, miR-182. We found that the high expression of miR-182 and miR-381 in gliomas are involved in pathological malignant progression. The silencing of miR-182 and miR-381 inhibited the proliferation <i>in vitro</i> and growth of glioma cell with <i>in vivo</i> magnetic resonance imaging by intracranial transplanted tumor model in rats. We also demonstrated that BRD7, a transcriptional cofactor for p53, is highly expressed and negatively correlated with <i>LRRC4</i> expression in gliomas. Disturbing miR-182 and miR-381 affected transcriptional regulation of the <i>BRD7</i> gene. This finding was verified by ectopic overexpression of <i>LRRC4</i> or restoration of endogenous <i>LRRC4</i> expression by treatment with the DNA demethylating agent 5-Aza-dC. Taken together, miR-182 and miR-381 may be a useful therapeutic target for treatment of glioma.</p></div
