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Updated: Mar 22, 2026
Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
Ampelopsin suppresses TNF-α-induced migration and invasion of U2OS osteosarcoma cells
Changying Liu1, Pengfei Zhao2, Yubao Yang1
1Department of Osteology, People's Hospital of Linyi City, Linyi, Shandong 276000, P.R. China.
Abstract:
Ampelopsin has been suggested as a novel anticancer agent, however, there is no evidence regarding its direct effect on the migration and invasion of osteosarcoma cells. The aims of the present study were to investigate the influence of ampelopsin on the migration and invasion of osteosarcoma cells and to clarify the underlying mechanisms. Scratch wound healing and Transwell assays were used to measure the migratory and invasive activities of the cells, respectively. The protein and RNA levels of matrix metalloproteinase-2 (MMP-2) were detected with western blot and RT-qPCR, respectively, following stimulation with tumor necrosis factor‑α (TNF-α) and ampelopsin. The expression levels of phospho‑ and total-p38MAPK were detected using western blot analysis. Additionally, SB203580, an inhibitor of p38MAPK, was used to investigate the effect of TNF‑α and ampelopsin. The results demonstrated that TNF‑α upregulated the expression level of MMP‑2 and promoted the migration and invasion of osteosarcoma cells. TNF‑α also activated the p38MAPK pathway, and SB203580 significantly inhibited the effect of TNF‑α on MMP‑2 expression. The application of ampelopsin abolished the effects of TNF‑α on the activation of the p38MAPK pathway and the expression of MMP‑2, and downregulated the migration and invasion of the osteosarcoma cells. These results demonstrated that ampelopsin inhibits the TNF‑α‑induced migration and invasion of osteosarcoma cells, and that the effect of ampelopsin was mediated by p38MAPK/MMP‑2 signaling.
Insights
Ampelopsin inhibits osteosarcoma cell migration and invasion by blocking the p38MAPK/MMP-2 pathway. This study clarifies ampelopsin
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Osteosarcoma is a primary bone cancer with significant metastatic potential.
- Ampelopsin is a plant-derived compound with proposed anticancer properties.
- The effect of ampelopsin on osteosarcoma cell migration and invasion remains uncharacterized.
Purpose of the Study:
- To investigate the impact of ampelopsin on osteosarcoma cell migration and invasion.
- To elucidate the molecular mechanisms underlying ampelopsin's effects.
- To determine if ampelopsin affects the p38MAPK/MMP-2 signaling pathway.
Main Methods:
- Scratch wound healing and Transwell assays were employed to assess cell migration and invasion.
- Western blot and RT-qPCR were used to measure matrix metalloproteinase-2 (MMP-2) protein and RNA levels.
- The p38MAPK pathway activation was analyzed via western blot for phospho- and total-p38MAPK.
- SB203580, a p38MAPK inhibitor, was utilized to validate pathway involvement.
Main Results:
- Tumor necrosis factor-α (TNF-α) upregulated MMP-2 expression, enhancing osteosarcoma cell migration and invasion.
- TNF-α activated the p38MAPK pathway, which was confirmed by inhibition with SB203580.
- Ampelopsin counteracted TNF-α's effects, reducing MMP-2 expression and inhibiting cell migration and invasion.
- Ampelopsin's action involved the suppression of TNF-α-induced p38MAPK pathway activation.
Conclusions:
- Ampelopsin effectively inhibits the migration and invasion of osteosarcoma cells.
- The inhibitory effects of ampelopsin are mediated through the p38MAPK/MMP-2 signaling pathway.
- Ampelopsin demonstrates potential as an anticancer agent for osteosarcoma treatment by targeting key metastatic pathways.
