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miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT

  • Authors:
    • Jing Zhou
    • Guobo Du
    • Hongmei Fu
  • View Affiliations / Copyright

    Affiliations: Department of Neurology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China, Department of Oncology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2151-2161
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    Published online on: March 3, 2020
       https://doi.org/10.3892/mmr.2020.11011
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Abstract

MicroRNAs (miRNA/miRs) serve an important function in the regulation of gene expression, and have been indicated to mediate a number of cellular biological processes, including cell proliferation, the cell cycle, cell apoptosis and cell differentiation. The altered expression of miRNAs has been revealed to result in a variety of human diseases, including glioblastoma multiforme (GBM). The present study indicated an increase in miR‑296‑3p in glioma tumor types compared with normal brain, particularly in the samples from patients with high grade GBM. Antagonizing miR‑296‑3p was demonstrated to induce cell growth arrest and cell cycle redistribution in U251 cells. The miR‑296‑3p antagonist altered the expression of a number of key genes that are involved in cell cycle control, including cyclin D1 and p21. Additionally, the decrease of miR‑296‑3p increased inhibitor of β‑catenin and T cell factor (ICAT) expression, and increased miR‑296‑3p‑inhibited ICAT expression in U251 cells. Bioinformatics analysis indicated that ICAT is a target gene of miR‑296‑3p, which was further validated using a dual‑luciferase reporter assay. Through the regulation of ICAT, the miR‑296‑3p antagonist decreased β‑catenin protein expression and increased the expression of its target genes. Silencing ICAT was indicated to reverse the miR‑296‑3p downregulation‑induced inactivation of Wnt signaling and cell growth arrest in glioma cells. The present study also indicated a negative correlation between ICAT mRNA levels and miR‑296‑3p levels in glioma tumor types. In conclusion, the present study identified an oncogenic function of miR‑296‑3p in glioblastoma via the direct regulation of ICAT.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou J, Du G and Fu H: miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT. Mol Med Rep 21: 2151-2161, 2020.
APA
Zhou, J., Du, G., & Fu, H. (2020). miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT. Molecular Medicine Reports, 21, 2151-2161. https://doi.org/10.3892/mmr.2020.11011
MLA
Zhou, J., Du, G., Fu, H."miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT". Molecular Medicine Reports 21.5 (2020): 2151-2161.
Chicago
Zhou, J., Du, G., Fu, H."miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT". Molecular Medicine Reports 21, no. 5 (2020): 2151-2161. https://doi.org/10.3892/mmr.2020.11011
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou J, Du G and Fu H: miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT. Mol Med Rep 21: 2151-2161, 2020.
APA
Zhou, J., Du, G., & Fu, H. (2020). miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT. Molecular Medicine Reports, 21, 2151-2161. https://doi.org/10.3892/mmr.2020.11011
MLA
Zhou, J., Du, G., Fu, H."miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT". Molecular Medicine Reports 21.5 (2020): 2151-2161.
Chicago
Zhou, J., Du, G., Fu, H."miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT". Molecular Medicine Reports 21, no. 5 (2020): 2151-2161. https://doi.org/10.3892/mmr.2020.11011
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