Long non-coding RNA SPRY4-IT1 promotes the proliferation and invasion of U251 cells through upregulation of SKA2

  • Authors:
    • Xiao‑Jun He
    • Er‑Bao Bian
    • Chun‑Chun Ma
    • Chao Wang
    • Hong‑Liang Wang
    • Bing Zhao
  • View Affiliations

  • Published online on: January 12, 2018     https://doi.org/10.3892/ol.2018.7776
  • Pages:3977-3984
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Abstract

The long non-coding RNA SPRY4-intronic transcript 1 (SPRY4-IT1) has been shown to promote the progression of cancer; however, the role of SPRY4‑IT1 in glioma remains unclear. The present study demonstrated that SPRY4‑IT1 expression was markedly increased in glioma tissues and cells compared with normal brain tissues, whereas knockdown of SPRY4‑IT1 inhibited cell proliferation, migration, and invasion in U251 cells. Spindle and kinetochore associated complex subunit 2 (SKA2) was found to be a target of SPRY4‑IT1 and was downregulated by SPRY4‑IT1‑knockdown. Additionally, SPRY4‑IT1 expression was positively correlated with SKA2 in glioma tissues. To the best of our knowledge, the present study provides the first demonstration that SKA2 may have an oncogenic role in U251 cells. These results indicate that SPRY4‑IT1 may serve a notable role in the molecular etiology of glioma and represents a potential target in glioma therapy.

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March 2018
Volume 15 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

2016 Impact Factor: 1.39
Ranked #68/217 Oncology
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APA
He, X., Bian, E., Ma, C., Wang, C., Wang, H., & Zhao, B. (2018). Long non-coding RNA SPRY4-IT1 promotes the proliferation and invasion of U251 cells through upregulation of SKA2. Oncology Letters, 15, 3977-3984. https://doi.org/10.3892/ol.2018.7776
MLA
He, X., Bian, E., Ma, C., Wang, C., Wang, H., Zhao, B."Long non-coding RNA SPRY4-IT1 promotes the proliferation and invasion of U251 cells through upregulation of SKA2". Oncology Letters 15.3 (2018): 3977-3984.
Chicago
He, X., Bian, E., Ma, C., Wang, C., Wang, H., Zhao, B."Long non-coding RNA SPRY4-IT1 promotes the proliferation and invasion of U251 cells through upregulation of SKA2". Oncology Letters 15, no. 3 (2018): 3977-3984. https://doi.org/10.3892/ol.2018.7776