Hydroxygenkwanin suppresses proliferation, invasion and migration of osteosarcoma cells via the miR‑320a/SOX9 axis
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Updated: Sep 2, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
Xinli Dong1, Yanhua Wang2, Hua Zhuang1
1Department of Orthopedics, Traditional Chinese Medicine Hospital of Binzhou, Binzhou, Shandong 256600, P.R. China.
Abstract:
Hydroxygenkwanin (HGK) has an anticancer effect in a variety of tumors, but its role in osteosarcoma has not been explored. The purpose of the present study was to investigate the therapeutic effect of HGK on osteosarcoma and its specific molecular mechanism. Osteosarcoma cells (MG‑63 and U2OS) treated with various concentrations of HGK were assigned to the treatment group. MTT, clone formation, wound healing and Transwell assays were performed to assess the viability, proliferation, migration, and invasion of MG‑63 and U2OS cells. RT‑qPCR was conducted to quantify the expression levels of of microRNA (miR)‑320a and SRY‑box transcription factor 9 (SOX9) in MG‑63 and U2OS cells. The binding sites of miR‑320a and SOX9 were predicted by starBase database, and verified using the dual‑luciferase reporter assay. The expression levels of SOX9 and EMT‑related proteins (N‑cadherin, E‑cadherin and vimentin) were detected by western blot analysis. HGK inhibited cell proliferation, migration, invasion, but promoted the expression of miR‑320a in MG‑63 and U2OS cells. Downregulation of miR‑320a reversed the effects of HGK on proliferation, migration and invasion of MG‑63 and U2OS cells, while upregulation of miR‑320a had the opposite effect. HGK inhibited the expression of SOX9 by promoting the expression of miR‑320a. Upregulation of SOX9 could partially reverse miR‑320a‑induced migration and invasion of MG‑63 and U2OS cells. In addition, upregulation of miR‑320a promoted E‑cadherin expression and inhibited the expression of N‑cadherin and vimentin, and the effect of miR‑320a was also reversed by SOX9. In conclusion, HGK inhibited proliferation, migration and invasion of MG‑63 and U2OS cells through the miR‑320a/SOX9 axis.
Insights
Hydroxygenkwanin (HGK) inhibits osteosarcoma cell growth and spread by increasing microRNA-320a (miR-320a) and decreasing SOX9. This study reveals HGK
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Hydroxygenkwanin (HGK) exhibits anticancer properties in various tumors.
- The therapeutic potential of HGK in osteosarcoma remains unexplored.
- Understanding HGK's molecular mechanisms is crucial for its clinical application.
Purpose of the Study:
- To investigate the therapeutic effects of HGK on osteosarcoma.
- To elucidate the specific molecular mechanisms underlying HGK's action in osteosarcoma.
- To explore the role of the miR-320a/SOX9 axis in HGK-mediated osteosarcoma inhibition.
Main Methods:
- Osteosarcoma cell lines (MG-63, U2OS) were treated with HGK.
- Cell viability, proliferation, migration, and invasion were assessed using MTT, clone formation, wound healing, and Transwell assays.
- Expression levels of miR-320a, SOX9, and EMT-related proteins were analyzed via RT-qPCR and Western blot.
Main Results:
- HGK inhibited osteosarcoma cell proliferation, migration, and invasion.
- HGK treatment upregulated miR-320a expression and downregulated SOX9 expression.
- The miR-320a/SOX9 axis was identified as a key mediator of HGK's anti-osteosarcoma effects.
Conclusions:
- HGK demonstrates significant therapeutic potential against osteosarcoma.
- HGK exerts its anti-cancer effects by modulating the miR-320a/SOX9 signaling pathway.
- Targeting the miR-320a/SOX9 axis could be a promising strategy for osteosarcoma treatment.
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