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Article Open Access

Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p

  • Authors:
    • Hui Yang
    • Weida Chen
    • Guangyu Jiang
    • Jun Yang
    • Weifeng Wang
    • Hongbin Li
  • View Affiliations / Copyright

    Affiliations: Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang 154001, P.R. China, Department of Cardiology, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang 154001, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang 154001, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1846-1854
    |
    Published online on: June 9, 2020
       https://doi.org/10.3892/ol.2020.11716
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Abstract

Long non-coding RNAs (lncRNA) are a type of ncRNA with a length ranging from 200‑1,000 nucleotides. Previous studies have confirmed that the lncRNA Ewing sarcoma associated transcript 1 (EWSAT1) exerts regulatory roles in cancer development and progression. However, its clinical significance in glioma remains unknown. In the present study, RNA‑sequencing data from the Gene Expression Omnibus database and The Cancer Genome Atlas was explored to investigate the association between EWSAT1 expression and prognosis in patients with glioma. Increased EWSAT1 was associated with the presence of necrosis on magnetic resonance imaging scans in patients with glioma. Furthermore, knockdown of EWSAT1 was indicated to suppress the proliferative and invasive abilities of glioblastoma cell lines using Cell Counting Kit‑8 and Transwell assays. Additionally, microRNA (miR)‑152‑3p was identified as a potential target of EWSAT1. The present study demonstrated that EWSAT1 interacted directly with miR‑152‑3p, and rescue experiments confirmed that EWSAT1 participated in glioma development by suppressing miR‑152‑3p. These results indicated that EWSAT1 is involved in the occurrence and progression of glioma, and may serve as a novel target and potential prognostic biomarker of glioma treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Yang H, Chen W, Jiang G, Yang J, Wang W and Li H: Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p. Oncol Lett 20: 1846-1854, 2020.
APA
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., & Li, H. (2020). Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p. Oncology Letters, 20, 1846-1854. https://doi.org/10.3892/ol.2020.11716
MLA
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., Li, H."Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p". Oncology Letters 20.2 (2020): 1846-1854.
Chicago
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., Li, H."Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p". Oncology Letters 20, no. 2 (2020): 1846-1854. https://doi.org/10.3892/ol.2020.11716
Copy and paste a formatted citation
x
Spandidos Publications style
Yang H, Chen W, Jiang G, Yang J, Wang W and Li H: Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p. Oncol Lett 20: 1846-1854, 2020.
APA
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., & Li, H. (2020). Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p. Oncology Letters, 20, 1846-1854. https://doi.org/10.3892/ol.2020.11716
MLA
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., Li, H."Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p". Oncology Letters 20.2 (2020): 1846-1854.
Chicago
Yang, H., Chen, W., Jiang, G., Yang, J., Wang, W., Li, H."Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p". Oncology Letters 20, no. 2 (2020): 1846-1854. https://doi.org/10.3892/ol.2020.11716
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