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

机译:德克梅哌咪唑抑制骨肉瘤细胞增殖和迁移,并通过调节miR-520a-3p来促进细胞凋亡

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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-ER K1/2. 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.
机译:该研究旨在探讨右甲酰甲基(DEX)对Osteosarcoma(OS)细胞系MG63的影响,并探讨OS中DEX和MIR-520-3P的可能关系。 结果表明,DEX可以上调MIR-520-3P,直接靶向AKT1。 另外,miR-520-3p还抑制了Mg63细胞增殖和迁移,促进的凋亡和抑制Akt,p-Akt,p-mtor和P-ER K1 / 2的蛋白表达。 德克斯可以通过上调miR-520a-3p的表达水平来抑制OS细胞增殖和迁移并促进细胞凋亡。 DEX可以用作OS治疗中的潜在治疗剂,MIR-520A-3P可以是OS治疗的潜在靶标。

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