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Decreased fibronectin expression in Met/HGF-mediated tumorigenesis
G A Taylor1, M Jeffers, C P Webb
1ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA.
Oncogene
|October 9, 1998
Summary
The Met receptor and hepatocyte growth factor (HGF) signaling significantly reduce fibronectin production in cancer cells, impacting tumor growth and spread. This decrease correlates with, but is not essential for, Met/HGF-driven cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The Met receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF)/scatter factor, are implicated in human cancer development and progression.
- Coexpression of Met and HGF in mesenchymal cells enhances cellular tumorigenic and metastatic potential.
Purpose of the Study:
- To identify gene expression changes induced by Met/HGF signaling that contribute to cancer phenotypes.
- To investigate the role of fibronectin in Met/HGF-mediated tumorigenesis.
Main Methods:
- Differential display screening was employed to detect gene expression alterations.
- Quantitative analysis of fibronectin mRNA and protein levels in cell lines and tumor samples.
Main Results:
- Met/HGF signaling led to a significant reduction in fibronectin mRNA and protein levels across multiple human and mouse tumor cell lines.
- A progressive decrease in fibronectin was observed in tumor explants and metastases from Met/HGF-transformed cells.
- Absence of fibronectin expression, a known cancer phenotype, was found to correlate with, but not be essential for, Met/HGF-driven tumorigenesis.
Conclusions:
- Met/HGF signaling modulates fibronectin expression, contributing to cancer progression.
- Fibronectin downregulation is associated with, but not a prerequisite for, Met/HGF-mediated tumor development and metastasis.