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Updated: Nov 19, 2025

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
Dexmedetomidine inhibits cell malignancy in osteosarcoma cells via miR-520a-3p-YOD1 interactome
Rongrong Yan1, Shuangfen Jin1, Hongchao Liu1
1Department of Anesthesiology, Maternal and Child Health Hospital of Hubei Province, Wuhan, Hubei, 430070, China.
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.
Insights
Dexmedetomidine (DEX) inhibits osteosarcoma progression by targeting the miR-520a-3p/YOD1 pathway. This study reveals DEX upregulates miR-520a-3p, suppressing YOD1 and reducing cancer cell malignancy.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Osteosarcoma is a prevalent adolescent cancer with poor survival rates.
- Dexmedetomidine (DEX) is used in osteosarcoma surgery.
- Aberrant miR-520a-3p and YOD1 expression is observed in osteosarcoma.
Purpose of the Study:
- To investigate the role of DEX in osteosarcoma progression.
- To explore the miR-520a-3p-YOD1 interaction in DEX-treated osteosarcoma cells.
Main Methods:
- Cell viability, proliferation, adhesion, and apoptosis assays (CCK-8, BrdU).
- Quantitative real-time PCR (RT-qPCR) and Western blotting to assess miR-520a-3p and YOD1 levels.
Main Results:
- DEX inhibited osteosarcoma cell viability, proliferation, and adhesion, while promoting apoptosis.
- miR-520a-3p targeted YOD1, suppressing osteosarcoma cell malignancy.
- DEX upregulated miR-520a-3p, inhibiting YOD1 expression and osteosarcoma cell malignancy.
Conclusions:
- DEX suppresses osteosarcoma cell malignancy through the miR-520a-3p/YOD1 axis.
- This pathway represents a potential therapeutic target for osteosarcoma treatment.
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