Open Access

ARTICLE

Overexpression of MicroRNA-216a Suppresses Proliferation, Migration, and Invasion of Glioma Cells by Targeting Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 5

Junfeng Zhang^*1, Kun Xu^†1, Lili Shi^*, Li Zhang^*, Zhaohua Zhao^*, Hao Xu^*, Fei Liang^*, Hongbo Li^*, Yan Zhao^*, Xi Xu^*, Yingfang Tian^‡

* Department of Human Anatomy, Xi’an Medical University, Xi’an, Shaanxi, P.R. China
† Department of Ophthalmology, The No.1 Hospital of Xi’an, Xi’an, Shaanxi, P.R. China
‡ College of Life Sciences, Shaanxi Normal University, Xi’an, Shaanxi, P.R. China
1 These authors provided equal contribution to this work and are co-first authors.

Oncology Research 2017, 25(8), 1317-1327. https://doi.org/10.3727/096504017X14874323871217

Abstract

Increasing studies have suggested that microRNAs (miRNAs) are involved in the development of gliomas. MicroRNA-216a has been reported to be a tumor-associated miRNA in many types of cancer, either as an oncogene or as a tumor suppressor. However, little is known about the function of miR-216a in gliomas. The present study was designed to explore the potential role of miR-216a in gliomas. We found that miR-216a was significantly decreased in glioma tissues and cell lines. Overexpression of miR-216a significantly suppressed the proliferation, migration, and invasion of glioma cells. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) was identified as a target gene of miR-216a in glioma cells by bioinformatics analysis, dual-luciferase reporter assay, real-time quantitative polymerase chain reaction, and Western blot analysis. Moreover, miR-216a overexpression inhibited the Wnt/β-catenin signaling pathway. The restoration of LGR5 expression markedly reversed the antitumor effect of miR-216a in glioma cells. Taken together, these findings suggest a tumor suppressor role for miR-216a in gliomas, which inhibits glioma cell proliferation, migration, and invasion by targeting LGR5. Our study suggests that miR-216a may serve as a potential therapeutic target for future glioma treatment.

---

Keywords

---