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Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A

  • Authors:
    • Xiongwu Yu
    • Weimin Wang
  • View Affiliations / Copyright

    Affiliations: Department of Pediatric Surgery, Maternal and Child Health‑Care Hospital of Qujing, Qujing, Yunnan 650032, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China
    Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 6729-6735
    |
    Published online on: September 5, 2017
       https://doi.org/10.3892/mmr.2017.7422
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Abstract

MicroRNAs (miRNAs) are small non‑coding RNAs which can serve as oncogenes or tumor suppressors in glioma. The present study aimed to investigate the expression of miR‑613 in glioma. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to detect miR‑613 in glioma cells and tissues and the relationship between miR‑613 and vascular endothelial growth factor (VEGF) A was assessed using a luciferase reporter assay. In addition, glioma cells were transfected with miR‑613 mimics and the mRNA and protein expression of VEGFA was detected using RT‑qPCR and western blot analysis, respectively. The proliferative, invasive and tube formation capabilities of transfected cells were also assessed in vitro. Furthermore, a nude mouse tumor xenograft model was used to investigate the effects of miR‑613 on tumor growth in vivo. The results of the present study demonstrated that the expression of miR‑613 was decreased in glioma cell lines, and was associated with the grade of glioma. Ectopic expression of miR‑613 markedly suppressed glioma cell proliferation and angiogenesis. Furthermore, the upregulation of miR‑613 inhibited tumor angiogenesis and tumor growth in xenografted nude mice in vivo. VEGFA was demonstrated as a direct target of miR‑613, as detected by western blot and luciferase reporter assays, and mediated miR‑613 induced glioma cell proliferation and angiogenesis inhibition.
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Copy and paste a formatted citation
Spandidos Publications style
Yu X and Wang W: Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A. Mol Med Rep 16: 6729-6735, 2017.
APA
Yu, X., & Wang, W. (2017). Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A. Molecular Medicine Reports, 16, 6729-6735. https://doi.org/10.3892/mmr.2017.7422
MLA
Yu, X., Wang, W."Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A". Molecular Medicine Reports 16.5 (2017): 6729-6735.
Chicago
Yu, X., Wang, W."Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A". Molecular Medicine Reports 16, no. 5 (2017): 6729-6735. https://doi.org/10.3892/mmr.2017.7422
Copy and paste a formatted citation
x
Spandidos Publications style
Yu X and Wang W: Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A. Mol Med Rep 16: 6729-6735, 2017.
APA
Yu, X., & Wang, W. (2017). Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A. Molecular Medicine Reports, 16, 6729-6735. https://doi.org/10.3892/mmr.2017.7422
MLA
Yu, X., Wang, W."Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A". Molecular Medicine Reports 16.5 (2017): 6729-6735.
Chicago
Yu, X., Wang, W."Tumor suppressor microRNA‑613 inhibits glioma cell proliferation, invasion and angiogenesis by targeting vascular endothelial growth factor A". Molecular Medicine Reports 16, no. 5 (2017): 6729-6735. https://doi.org/10.3892/mmr.2017.7422
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