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Published on: October 28, 2021
Sevoflurane Inhibited Osteosarcoma Cell Proliferation And Invasion Via Targeting miR-203/WNT2B/Wnt/β-Catenin Axis
Meixian Chen1, Lisheng Zhou1, Zhaoxia Liao1
1Department of Anesthesiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, People's Republic of China.
Background:
Osteosarcoma is one of the most common primary bone cancers with predominant occurrence in children and adolescents. This study aimed to determine the effects of sevoflurane treatment on the osteosarcoma progression and to explore the underlying molecular mechanisms.
Materials And Methods:
The mRNA and protein expression levels were determined by qPCR and Western blot, respectively. Osteosarcoma cell proliferation, apoptosis and invasion were determined by MTT, caspase-3 activity, colony formation and Transwell invasion assays, respectively. The interaction between miR-203 and WNT2B 3' untranslated region was confirmed by luciferase reporter assay.
Results:
Sevoflurane treatment for 6 hrs concentration-dependently suppressed cell viability, increased caspase-3 activity and up-regulated miR-203 expression in both U2OS and MG63 cells. MiR-203 overexpression suppressed cell viability, increased caspase-3 activity and suppressed cell growth and invasion of osteosarcoma cells. In addition, miR-203 knockdown attenuated the tumor-suppressive effects of sevoflurane treatment on osteosarcoma cells. Mechanistic studies showed that miR-203 repressed the expression of WNT2B in U2OS cells, and inhibition of miR-203 attenuated the suppressive effects of sevoflurane on WNT2B expression. More importantly, WNT2B overexpression attenuated the effects of sevoflurane treatment on cell viability, caspase-3 activity, cell growth and invasion of U2OS cells. MiR-203 overexpression suppressed Wnt/β-catenin signalling. Similarly, sevoflurane suppressed the activity of Wnt/β-catenin signalling, which was partially reversed by miR-203 knockdown and WTN2B overexpression.
Conclusion:
Our data showed the tumor-suppressive effects of sevoflurane on osteosarcoma cells, and mechanistic studies revealed that sevoflurane inhibited osteosarcoma cell proliferation and invasion partly via targeting the miR-203/WNT2B/Wnt/β-catenin axis.
Insights
Sevoflurane suppresses osteosarcoma progression by up-regulating miR-203, inhibiting WNT2B, and down-regulating the Wnt/β-catenin pathway. This study reveals sevoflurane
Area of Science:
- Oncology
- Molecular Biology
- Anesthesiology
Background:
- Osteosarcoma is a prevalent bone cancer in children and adolescents.
- Understanding sevoflurane's impact on osteosarcoma is crucial for treatment strategies.
Purpose of the Study:
- To investigate the effects of sevoflurane on osteosarcoma progression.
- To elucidate the molecular mechanisms underlying sevoflurane's action.
Main Methods:
- Quantitative PCR (qPCR) and Western blot for gene and protein expression.
- MTT, caspase-3 activity, colony formation, and Transwell assays for cell behavior.
- Luciferase reporter assay to confirm miR-203 and WNT2B interaction.
Main Results:
- Sevoflurane suppressed osteosarcoma cell viability, increased apoptosis, and upregulated miR-203.
- miR-203 overexpression mimicked sevoflurane's effects, inhibiting proliferation and invasion.
- Sevoflurane targets the miR-203/WNT2B/Wnt/β-catenin axis, suppressing tumor growth.
Conclusions:
- Sevoflurane exhibits tumor-suppressive effects on osteosarcoma cells.
- The miR-203/WNT2B/Wnt/β-catenin pathway is a key mechanism for sevoflurane's action.
- Sevoflurane holds potential as a therapeutic agent for osteosarcoma.
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