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Updated: Jan 22, 2026

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Published on: November 29, 2016
Suppression of ERK/NF-κB Activation Is Associated With Amentoflavone-Inhibited Osteosarcoma Progression In Vivo
Yen-Ju Lee1,2, Jing-Gung Chung3,4, Yi-Ting Chien5
1Department of Emergency Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C.
Background/Aim:
Amentoflavone has been implicated in reducing the metastatic potential of osteosarcoma (OS) cells in vitro. The aim of the present study was to verify the antitumoral efficacy and the potential mechanism of amentoflavone osteosarcoma progression inhibition in vivo.
Materials And Methods:
A U-2 OS osteosarcoma xenograft mouse model was used in this study. Mice were treated with a vehicle control or amentoflavone (100 mg/kg/day) for 15 days. Tumor growth, signal transduction, and expression of tumor progression-associated proteins were evaluated using a digital caliper, bioluminescence imaging (BLI), animal computed tomography (CT), and ex vivo western blotting assay.
Results:
Amentoflavone significantly inhibits tumor growth and reduces protein levels of phospho-extracellular signal-regulated kinase (P-ERK), nuclear factor-kappaB (NF-κB) p65 (Ser536), vascular endothelial growth factor (VEGF), matrix metallopeptidase 9 (MMP-9), X-linked inhibitor of apoptosis protein (XIAP), and cyclin-D1 in osteosarcoma in vivo.
Conclusion:
The inhibition of ERK/NF-κB activation is associated with amentoflavone-inhibited osteosarcoma progression in vivo.
Insights
Amentoflavone effectively inhibits osteosarcoma (OS) tumor growth in vivo. This natural compound reduces key proteins involved in cancer progression by inhibiting the ERK/NF-κB signaling pathway.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Osteosarcoma (OS) is a primary bone cancer with high metastatic potential.
- Amentoflavone, a natural flavonoid, has shown promise in inhibiting OS cell metastasis in vitro.
- Further investigation is needed to confirm its efficacy and mechanism in vivo.
Purpose of the Study:
- To evaluate the antitumoral efficacy of amentoflavone in an in vivo osteosarcoma model.
- To elucidate the molecular mechanisms underlying amentoflavone's inhibitory effects on osteosarcoma progression.
Main Methods:
- Amentoflavone (100 mg/kg/day) or vehicle control was administered to mice with U-2 OS osteosarcoma xenografts for 15 days.
- Tumor growth was monitored using digital calipers and bioluminescence imaging (BLI).
- Signal transduction and protein expression (P-ERK, NF-κB, VEGF, MMP-9, XIAP, cyclin-D1) were assessed via western blotting.
Main Results:
- Amentoflavone significantly suppressed osteosarcoma tumor growth in vivo.
- Treatment reduced protein levels of phospho-extracellular signal-regulated kinase (P-ERK), nuclear factor-kappaB (NF-κB) p65, vascular endothelial growth factor (VEGF), matrix metallopeptidase 9 (MMP-9), X-linked inhibitor of apoptosis protein (XIAP), and cyclin-D1.
- These findings suggest amentoflavone impacts multiple pathways crucial for tumor progression.
Conclusions:
- Amentoflavone demonstrates significant in vivo antitumoral efficacy against osteosarcoma.
- The observed inhibition of osteosarcoma progression is linked to the suppression of ERK/NF-κB signaling pathways.
- Amentoflavone represents a potential therapeutic agent for osteosarcoma treatment.
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