Open Access

Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway

  • Authors:
    • Xiao‑Xue Ke
    • Yi Pang
    • Kuijun Chen
    • Dunke Zhang
    • Feng Wang
    • Shunqin Zhu
    • Jingxin Mao
    • Xiaosong Hu
    • Guanghui Zhang
    • Hongjuan Cui
  • View Affiliations

  • Published online on: October 9, 2018     https://doi.org/10.3892/or.2018.6777
  • Pages: 3313-3322
  • Copyright: © Ke et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

It is generally known that glioblastoma is the most common primary malignant brain tumor and that it is highly aggressive and deadly. Although surgical and pharmacological therapies have made long‑term progress, glioblastoma remains extremely lethal and has an uncommonly low survival rate. Therefore, further elucidation of the molecular mechanisms of glioblastoma initiation and its pathological processes are urgent. Arsenic resistance protein 2 (Ars2) is a highly conserved gene, and it has been found to play an important role in microRNA biosynthesis and cell proliferation in recent years. Furthermore, absence of Ars2 results in developmental death in Drosophila, zebrafish and mice. However, there are few studies on the role of Ars2 in regulating tumor development, and the mechanism of its action is mostly unknown. In the present study, we revealed that Ars2 is involved in glioblastoma proliferation and we identified a potential mechanistic role for it in cell cycle control. Our data demonstrated that Ars2 knockdown significantly repressed the proliferation and tumorigenesis abilities of glioblastoma cells in vitro and in vivo. Further investigation clarified that Ars2 deficiency inhibited the activation of the MAPK/ERK pathway, leading to cell cycle arrest in the G1 phase, resulting in suppression of cell proliferation. These findings support the conclusion that Ars2 is a key regulator of glioblastoma progression.
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December-2018
Volume 40 Issue 6

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Ke XX, Pang Y, Chen K, Zhang D, Wang F, Zhu S, Mao J, Hu X, Zhang G, Cui H, Cui H, et al: Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway. Oncol Rep 40: 3313-3322, 2018
APA
Ke, X., Pang, Y., Chen, K., Zhang, D., Wang, F., Zhu, S. ... Cui, H. (2018). Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway. Oncology Reports, 40, 3313-3322. https://doi.org/10.3892/or.2018.6777
MLA
Ke, X., Pang, Y., Chen, K., Zhang, D., Wang, F., Zhu, S., Mao, J., Hu, X., Zhang, G., Cui, H."Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway". Oncology Reports 40.6 (2018): 3313-3322.
Chicago
Ke, X., Pang, Y., Chen, K., Zhang, D., Wang, F., Zhu, S., Mao, J., Hu, X., Zhang, G., Cui, H."Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway". Oncology Reports 40, no. 6 (2018): 3313-3322. https://doi.org/10.3892/or.2018.6777