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

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A Correction to this article was published on 22 October 2020

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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.

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Change history

  • 22 October 2020

    The original version of this article unfortunately contained a mistake in the AuthorGroup section.

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Acknowledgment

This work was supported by some other members in our lab.

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Correspondence to Maode Wang.

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The authors declare that they have no conflicts of interest.

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Hao, W., Luo, W., Bai, M. et al. MicroRNA-206 Inhibited the Progression of Glioblastoma Through BCL-2. J Mol Neurosci 60, 531–538 (2016). https://doi.org/10.1007/s12031-016-0824-6

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  • DOI: https://doi.org/10.1007/s12031-016-0824-6

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