期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 543, 期 -, 页码 56-64出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.01.045
关键词
Dexmedetomidine; miR-520a-3p; YOD1; Malignancy; Osteosarcoma; Proliferation
资金
- Joint Fund Project of Hubei Health Commission [WJ2019H284]
The study demonstrated that Dexmedetomidine inhibits the malignancy of osteosarcoma cells by upregulating miR-520a-3p to suppress YOD1 expression, suggesting a new potential therapeutic approach for osteosarcoma.
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-520a3p/YOD1 axis. (c) 2021 Elsevier Inc. All rights reserved.
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