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miR-22 inhibits the proliferation, motility, and invasion of human glioblastoma cells by directly targeting SIRT1

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Tumor Biology

Abstract

Recently, microRNAs (miRNAs), a kind of small and non-coding RNA, can target the downstream molecules. Increasing evidence demonstrates that miRNAs meditate the onset and progression of a variety of tumors. In the present study, we carried out gene transfection, western blot, and reverse transcription PCR (RT-PCR) to explore the role of miR-22 in glioblastoma tissues and cell lines. Here, we verified that the expression of miR-22 was downregulated in glioblastoma tissues and cells rather than matched non-tumor tissues and normal human astrocyte (NHA) cells (p < 0.001). By contrast, SIRT1 messenger RNA (mRNA) and protein were upregulated in glioblastoma tissues and cells (p < 0.001). In vitro miR-22 mimics interfered with cell proliferation, migration, and invasion of U87 and U251 cells. Mechanically, the 3′-untranslated regions (3′-UTRs) of SIRT1 were a direct target of miR-22, leading to the decreased expression of SIRT1 protein in U87 and U251 cells. Meanwhile, miR-22 mimics also inhibited the expression of epidermal growth factor receptor (EGFR) and matrix metallopeptidase 9 (MMP9). In conclusion, miR-22 inhibited cell proliferation, migration, and invasion via targeting the 3′-UTR of SIRT1 in the progression of glioblastoma and miR-22-SIRT1 pathway can be recommended as a potential target for treatment of glioblastoma.

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Acknowledgments

This work was supported by the National Natural Science Foundation of China (Project No. 81502163 and 31370810). We greatly thank Bo Hong in Department of Neurosurgery, Changhai Hospital, Second Military Medical University (Shanghai, 200433, P.R. China) for valuable suggestions and his fund.

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Correspondence to Dongwei Dai.

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Hanchun Chen and Qiong Lu contributed equally to this work.

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Chen, H., Lu, Q., Fei, X. et al. miR-22 inhibits the proliferation, motility, and invasion of human glioblastoma cells by directly targeting SIRT1. Tumor Biol. 37, 6761–6768 (2016). https://doi.org/10.1007/s13277-015-4575-8

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  • DOI: https://doi.org/10.1007/s13277-015-4575-8

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