右美托咪定通过 miR-520a-3p-YOD1 互作网络抑制骨肉瘤细胞的恶性表型。
Dexmedetomidine inhibits cell malignancy in osteosarcoma cells via miR-520a-3p-YOD1 interactome.
机构信息
Department of Anesthesiology, Maternal and Child Health Hospital of Hubei Province, Wuhan, Hubei, 430070, China.
Department of Anesthesiology, Maternal and Child Health Hospital of Hubei Province, Wuhan, Hubei, 430070, China.
出版信息
Biochem Biophys Res Commun. 2021 Mar 5;543:56-64. doi: 10.1016/j.bbrc.2021.01.045. Epub 2021 Jan 27.
BACKGROUND
Osteosarcoma is a common malignant tumor in adolescents with a low 5-year survival rate. Dexmedetomidine (DEX) has been widely used for surgery of osteosarcoma patients. MiR-520a-3p and YOD1 expression was abnormal in osteosarcoma cells. However, whether DEX affects osteosarcoma progression via miR-520a-3p-YOD1 interactome needs to be explored.
METHODS
We detected osteosarcoma cells biological behavior by CCK-8 assay, BrdU assay, cell adhesion assay, and apoptosis assay, respectively. The miR-520a-3p and YOD1 levels was explored in osteosarcoma cell lines by RT-qPCR or western blotting assay.
RESULTS
In this study, we found that DEX treating osteosarcoma cells inhibited cell viability, proliferation and adhesion, while it promoted cell apoptosis. Moreover, miR-520a-3p targeting to YOD1 also functionally repressed cell malignancy in osteosarcoma cells. Notably, DEX treatment could inhibit YOD1 expression via upregulating miR-520a-3p, thereby suppressing cell malignancy in osteosarcoma.
CONCLUSIONS
Our study first revealed that DEX inhibited malignancy of osteosarcoma cells via miR-520a-3p/YOD1 axis.
背景
骨肉瘤是青少年中常见的恶性肿瘤，5 年生存率较低。右美托咪定（DEX）已广泛用于骨肉瘤患者的手术。miR-520a-3p 和 YOD1 在骨肉瘤细胞中的表达异常。然而，DEX 是否通过 miR-520a-3p-YOD1 互作网络影响骨肉瘤进展仍需探索。
方法
我们分别通过 CCK-8 检测、BrdU 检测、细胞黏附实验和细胞凋亡实验检测骨肉瘤细胞的生物学行为。通过 RT-qPCR 或 Western blot 检测骨肉瘤细胞系中 miR-520a-3p 和 YOD1 的水平。
结果
本研究发现，DEX 处理骨肉瘤细胞可抑制细胞活力、增殖和黏附，促进细胞凋亡。此外，miR-520a-3p 靶向 YOD1 也可在骨肉瘤细胞中发挥功能抑制细胞恶性表型。值得注意的是，DEX 可通过上调 miR-520a-3p 抑制 YOD1 表达，从而抑制骨肉瘤细胞的恶性表型。
结论
本研究首次揭示了 DEX 通过 miR-520a-3p/YOD1 轴抑制骨肉瘤细胞的恶性程度。
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