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J Mol Neurosci. 2016 Dec;60(4):531-538. Epub 2016 Aug 25.

MicroRNA-206 Inhibited the Progression of Glioblastoma Through BCL-2.

Author information

1
Department of Neurosurgery, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China.
2
Department of Neurosurgery, Affiliated Hospital, Medical College of Yan'an University, Yan'an City, Shaanxi, 716000, People's Republic of China.
3
Department of Neurosurgery, The Affiliated Hospital of Shaanxi Traditional Chinese Medicine University, Xianyang, 712000, People's Republic of China.
4
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China.
5
Department of Neurosurgery, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China. maodewang@163.com.

Abstract

Gliomas are the most common type of brain tumor and have a poor prognosis. MicroRNAs (miRNAs) are a class of small, endogenous, and non-coding RNAs that play crucial roles in cell proliferation, survival, and invasion. Deregulated expression of miR-206 has been investigated in many cancers. However, the role of miR-206 in glioblastoma is still unclear. In the present study, we found that the expression of miR-206 was decreased in cancer tissues compared with normal tissues. However, the expression level of BCL-2 was higher in cancer tissues than that in normal tissues (all p < 0.001). Statistically, the expression level of BCL-2 was inversely correlated with the miR-206. In addition, the overall survival of glioblastoma patients with lower miR-206 expression was significantly shorter than those with high miR-206 expression (p < 0.001). Besides, the expression of miR-206 was also decreased in U87 and U251 cells. In vitro assays showed that ectopic miR-206 expression affected the proliferation, cell cycle, and invasion in U87 and U251 cells. Importantly, we identified BCL-2 as a direct target of miR-206 in U87 and U251 cells using luciferase assay. Overexpression of BCL-2 partially attenuated the miR-206-mediated cell proliferation. In vivo, overexpression of miR-206 suppressed the progression of glioblastoma cells using mice xenograft model. In conclusion, this study suggested that miR-206 could act as a tumor suppressor gene through inhibiting BCL-2 in the development of glioblastoma.

KEYWORDS:

BCL-2; Glioblastoma; Suppressor; miR-206

PMID:
27558109
DOI:
10.1007/s12031-016-0824-6
[Indexed for MEDLINE]

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