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Dexmedetomidine Inhibits Osteosarcoma Cell Proliferation and Migration, and Promotes Apoptosis by Regulating miR-520a-3p

Xiaoyan Wang*, Yongguang Xu*, Xinlei Chen*, Jianmin Xiao

* Department of Anesthesiology, Shandong Provincial Hospital Affiliated With Shandong University, Jinan, Shandong, P.R. China
† Department of Anesthesiology, Ningjin People’s Hospital, Ningjin, Shandong, P.R. China

Oncology Research 2018, 26(3), 495-502. https://doi.org/10.3727/096504017X14982578608217

Abstract

This study aimed to investigate the effect of dexmedetomidine (DEX) on osteosarcoma (OS) cell line MG63 and to explore the possible relationship between DEX and miR-520-3p in OS. The results showed that DEX could upregulate miR-520-3p, which directly targeted AKT1. Additionally, miR-520-3p also inhibited MG63 cell proliferation and migration, promoted apoptosis, and suppressed protein expressions of AKT, p-AKT, p-mTOR, and p-ERK1/2. DEX can inhibit OS cell proliferation and migration and promote apoptosis by upregulating the expression level of miR-520a-3p. DEX may serve as a potential therapeutic agent in OS treatment, and miR-520a-3p may be a potential target in the therapy of OS.

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Cite This Article

APA Style
Wang, X., Xu, Y., Chen, X., Xiao, J. (2018). Dexmedetomidine inhibits osteosarcoma cell proliferation and migration, and promotes apoptosis by regulating mir-520a-3p. Oncology Research, 26(3), 495-502. https://doi.org/10.3727/096504017X14982578608217
Vancouver Style
Wang X, Xu Y, Chen X, Xiao J. Dexmedetomidine inhibits osteosarcoma cell proliferation and migration, and promotes apoptosis by regulating mir-520a-3p. Oncol Res. 2018;26(3):495-502 https://doi.org/10.3727/096504017X14982578608217
IEEE Style
X. Wang, Y. Xu, X. Chen, and J. Xiao, “Dexmedetomidine Inhibits Osteosarcoma Cell Proliferation and Migration, and Promotes Apoptosis by Regulating miR-520a-3p,” Oncol. Res., vol. 26, no. 3, pp. 495-502, 2018. https://doi.org/10.3727/096504017X14982578608217



cc Copyright © 2018 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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