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Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
HGF and c-Met interaction promotes migration in human chondrosarcoma cells
Hsi-Kai Tsou1, Hsien-Te Chen, Ya-Huey Hung
1Department of Neurosurgery, Taichung Veterans General Hospital, Taichung, Taiwan.
Plos One
|January 16, 2013
Summary
Hepatocyte growth factor (HGF) drives chondrosarcoma cell migration and metastasis by increasing matrix metalloproteinase-2 (MMP-2) expression. Inhibiting the c-Met/PI3K/Akt/PKCδ/NF-κB pathway blocks this HGF-induced cell movement.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Chondrosarcoma is a malignant bone tumor known for local invasion and metastasis, frequently to the lungs.
- Hepatocyte growth factor (HGF) is implicated in cancer progression, but its role in chondrosarcoma cell migration is unclear.
Purpose of the Study:
- To investigate the effect of HGF on human chondrosarcoma cell migration and elucidate the underlying molecular mechanisms.
Main Methods:
- Analysis of HGF expression in human chondrosarcoma tissues and normal cartilage.
- Assessing the impact of HGF on chondrosarcoma cell migration and MMP-2 expression in vitro.
- Utilizing c-Met inhibitors, siRNA, and pathway-specific inhibitors (PI3K, Akt, PKCδ, NF-κB) to block HGF signaling.
Main Results:
- Human chondrosarcoma tissues showed significantly higher HGF expression than normal cartilage.
- HGF treatment increased chondrosarcoma cell migration and MMP-2 expression.
- Inhibition of c-Met, PI3K, Akt, PKCδ, or NF-κB abrogated HGF-induced cell migration and MMP-2 upregulation.
Conclusions:
- HGF promotes chondrosarcoma cell migration by upregulating MMP-2 expression.
- This process is mediated via the c-Met receptor and the PI3K/Akt/PKCδ/NF-κB signaling pathway.
- Targeting this pathway may offer therapeutic strategies for chondrosarcoma metastasis.
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