miR-188 Inhibits Glioma Cell Proliferation and Cell Cycle Progression Through Targeting beta-Catenin

摘要

MicroRNAs (miRNAs) play important roles in several human cancers. Although miR-188 has been suggested to function as a tumor repressor in cancers, its precise role in glioma and the molecular mechanism remain unknown. In the present study, we investigated the effect of miR-188 on glioma and explored its relevant mechanisms. We found that the expression of miR-188 is dramatically downregulated in glioma tissues and cell lines. Subsequent investigation revealed that miR-188 expression was inversely correlated with beta-catenin expression in glioma tissue samples. Using a luciferase reporter assay, beta-catenin was determined to be a direct target of miR-188. Overexpression of miR-188 reduced beta-catenin expression at both the mRNA and protein levels, and inhibition of miR-188 increased beta-catenin expression. Moreover, we found that overexpression of miR-188 suppressed glioma cell proliferation and cell cycle G(1)-S transition, whereas inhibition of miR-188 promoted glioma cell proliferation. Importantly, silencing b-catenin recapitulated the cellular and molecular effects seen upon miR-188 overexpression, which included inhibiting glioma cell proliferation and G(1)-S transition. Taken together, our results demonstrated that miR-188 inhibits glioma cell proliferation by targeting beta-catenin, representing an effective therapeutic strategy for glioma.