MicroRNA‑216b inhibits cell proliferation and invasion in glioma by directly targeting metadherin.

Glioma is a well‑known aggressive and malignant brain tumor, and accounts for ~30% of all brain and central nervous system tumors. A number of studies have indicated that the abnormal expression of specific microRNAs (miR) serves vital roles in the tumorigenesis and tumor development of human cancer, including glioma. miR‑216b has been studied in a number of types of cancer. However, the expression pattern, molecular function and underlying mechanisms of miR‑216b in glioma remain unclear. In the present study, it was demonstrated that the level of miR‑216b was significantly decreased in glioma tissues and cell lines compared with matched normal tissues and primary normal human astrocytes. The reduced miR‑216b expression level was correlated with the Karnofsky Performance Score and the World Health Organization grade of gliomas. Upregulation of miR‑216b repressed cell proliferation and invasion in glioma. Additionally, metadherin (MTDH) was identified as a direct target gene of miR‑216b in glioma. MTDH expression was demonstrated to be significantly upregulated and inversely associated with miR‑216b expression in glioma specimens. MTDH knockdowns could simulate the cellular conditions induced by miR‑216b overexpression in glioma cells. In addition, miR‑216b regulated phosphatidylinositol 3,4,5‑trisphosphate 3‑phosphatase and dual‑specificity protein phosphatase PTEN/protein kinase B signaling pathways in glioma. These results suggested that miR‑216b acted as a tumor suppressor in glioma by directly targeting MTDH and that the miR‑216b/MTDH axis may be an effective therapeutic target for the treatment of patients with this disease.