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MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3

  • Authors:
    • Xiaomei Mo
    • Qian Cao
    • Hui Liang
    • Jianmin Liu
    • Huahui Li
    • Fenghai Liu
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacy, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China, Heart Center, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China, Department of Hematology, Qingdao Women and Children Hospital, Qingdao, Shandong 266034, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China, Department of Laboratory Medicine of Qingdao Municipal Hospital, Qingdao, Shandong 266011, P.R. China
    Copyright: © Mo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1961-1966
    |
    Published online on: January 12, 2016
       https://doi.org/10.3892/mmr.2016.4760
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Abstract

Previous studies have shown that microRNA (miR)-610 is crucial in a variety of biological processes in various types of human cancer cells. However, the role of this microRNA in glioblastoma (GBM) is presently unclear. In this study, the role of miR‑610 in cell proliferation was investigated in GBM. It was demonstrated that miR‑610 expression is markedly downregulated in GBM cells and GBM tissues compared with normal human astrocytes (NHAs) and normal brain tissue, respectively. Ectopic expression of miR‑610 reduced the proliferation and anchorage‑independent growth of GBM cells, whereas inhibition of miR‑610 promoted this effect. Bioinformatics analysis further revealed cyclin D2 (CCND2) and AKT3, putative tumor promoters, as potential targets of miR‑610. Data from reporter assays showed that miR‑610 directly binds to the 3'‑untranslated region of CCND2 and AKT3 mRNA, and represses their expression at the transcriptional and translational levels. In conclusion, the data provide compelling evidence that miR‑610 functions as an anti‑onco‑miRNA, which is important in inhibiting cell proliferation in GBM, and its anti‑oncogenic effects are mediated chiefly through direct suppression of CCND2 and AKT3 expression.
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Copy and paste a formatted citation
Spandidos Publications style
Mo X, Cao Q, Liang H, Liu J, Li H and Liu F: MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3. Mol Med Rep 13: 1961-1966, 2016.
APA
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., & Liu, F. (2016). MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3. Molecular Medicine Reports, 13, 1961-1966. https://doi.org/10.3892/mmr.2016.4760
MLA
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., Liu, F."MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3". Molecular Medicine Reports 13.3 (2016): 1961-1966.
Chicago
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., Liu, F."MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3". Molecular Medicine Reports 13, no. 3 (2016): 1961-1966. https://doi.org/10.3892/mmr.2016.4760
Copy and paste a formatted citation
x
Spandidos Publications style
Mo X, Cao Q, Liang H, Liu J, Li H and Liu F: MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3. Mol Med Rep 13: 1961-1966, 2016.
APA
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., & Liu, F. (2016). MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3. Molecular Medicine Reports, 13, 1961-1966. https://doi.org/10.3892/mmr.2016.4760
MLA
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., Liu, F."MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3". Molecular Medicine Reports 13.3 (2016): 1961-1966.
Chicago
Mo, X., Cao, Q., Liang, H., Liu, J., Li, H., Liu, F."MicroRNA-610 suppresses the proliferation of human glioblastoma cells by repressing CCND2 and AKT3". Molecular Medicine Reports 13, no. 3 (2016): 1961-1966. https://doi.org/10.3892/mmr.2016.4760
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