Open Access

ARTICLE

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

Nan Li^*†, Hangyu Shi^†, Lu Zhang^‡, Xu Li^§, Lu Gao^†, Gang Zhang^†, Yongqiang Shi^†, Shiwen Guo^*

* Department of Neurosurgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, P.R. China
† Department of Neurosurgery, Xi’an Children’s Hospital, Xi’an, Shaanxi, P.R. China
‡ Department of Foreign Languages, Ming De College of Northwestern Polytechnical University, Xi’an, Shaanxi, P.R. China
§ Department of First Internal Medicine, Shaanxi Province Tumor Hospital, Xi’an, Shaanxi, P.R. China

Oncology Research 2018, 26(5), 785-794. https://doi.org/10.3727/096504017X15127309628257

Abstract

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 β-catenin expression in glioma tissue samples. Using a luciferase reporter assay, β-catenin was determined to be a direct target of miR-188. Overexpression of miR-188 reduced β-catenin expression at both the mRNA and protein levels, and inhibition of miR-188 increased β-catenin expression. Moreover, we found that overexpression of miR-188 suppressed glioma cell proliferation and cell cycle G₁–S transition, whereas inhibition of miR-188 promoted glioma cell proliferation. Importantly, silencing β-catenin recapitulated the cellular and molecular effects seen upon miR-188 overexpression, which included inhibiting glioma cell proliferation and G₁–S transition. Taken together, our results demonstrated that miR-188 inhibits glioma cell proliferation by targeting β-catenin, representing an effective therapeutic strategy for glioma.

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