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Article

miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1

Retraction in: /10.3892/or.2023.8663
  • Authors:
    • Tingting Zhang
    • Guangtao Ma
    • Yan Zhang
    • Hongda Huo
    • Yuqian Zhao
  • View Affiliations / Copyright

    Affiliations: School of Basic Medical Science, Central South University, Changsha, Hunan 410078, P.R. China, Department of Neurosurgery, Daqing Oil Field General Hospital, Daqing, Heilongjiang 163000, P.R. China, Department of The Heart of Non-Invasive Examination, Daqing Oil Field General Hospital, Daqing, Heilongjiang 163000, P.R. China, Daqing Convalescence Hospital, Daqing, Heilongjiang 163000, P.R. China, School of Information Science and Engineering, Central South University, Changsha, Hunan 410078, P.R. China
  • Pages: 1751-1759
    |
    Published online on: July 17, 2017
       https://doi.org/10.3892/or.2017.5824
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Abstract

MicroRNAs (miRNAs) play a vital role in tumour biological and pathologic processes. In the present study, we aimed to detect the expression and biological role of miR-216b in glioma. Our data showed that miR-216b was significantly downregulated in human glioma tissues and cells. Ectopic expression of miR-216b inhibited the proliferation and invasion of U87 and U251 cells and suppressed the growth of xenograft tumours in vivo. Bioinformatic and luciferase reporter analyses identified Forkhead box protein M1 (FoxM1) as a direct target of miR-216b. Overexpression of miR-216b inhibited the expression of FoxM1 in glioma cells. Rescue experiments demonstrated that co-transfection of FoxM1 lacking the 3'-untranslated region partially prevented miR‑216b-induced inhibition of glioma cell growth and invasion. In vivo studies indicated that ectopic expression of miR-216b impeded the proliferation of glioma xenograft tumours in nude mice, coupled with a decreased in FoxM1 protein expression and the percentage of Ki-67-positive tumour cells. Taken together, our results provide evidence of the suppressive activity of miR‑216b in glioma, which is largely ascribed to downregulation of FoxM1. Restoration of miR-216b may provide a novel potential therapeutic agent for glioma.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang T, Ma G, Zhang Y, Huo H and Zhao Y: miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663. Oncol Rep 38: 1751-1759, 2017.
APA
Zhang, T., Ma, G., Zhang, Y., Huo, H., & Zhao, Y. (2017). miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663. Oncology Reports, 38, 1751-1759. https://doi.org/10.3892/or.2017.5824
MLA
Zhang, T., Ma, G., Zhang, Y., Huo, H., Zhao, Y."miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663". Oncology Reports 38.3 (2017): 1751-1759.
Chicago
Zhang, T., Ma, G., Zhang, Y., Huo, H., Zhao, Y."miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663". Oncology Reports 38, no. 3 (2017): 1751-1759. https://doi.org/10.3892/or.2017.5824
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang T, Ma G, Zhang Y, Huo H and Zhao Y: miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663. Oncol Rep 38: 1751-1759, 2017.
APA
Zhang, T., Ma, G., Zhang, Y., Huo, H., & Zhao, Y. (2017). miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663. Oncology Reports, 38, 1751-1759. https://doi.org/10.3892/or.2017.5824
MLA
Zhang, T., Ma, G., Zhang, Y., Huo, H., Zhao, Y."miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663". Oncology Reports 38.3 (2017): 1751-1759.
Chicago
Zhang, T., Ma, G., Zhang, Y., Huo, H., Zhao, Y."miR-216b inhibits glioma cell migration and invasion through suppression of FoxM1 Retraction in /10.3892/or.2023.8663". Oncology Reports 38, no. 3 (2017): 1751-1759. https://doi.org/10.3892/or.2017.5824
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