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Expression of the HGF/SF receptor, c-met, and its ligand in human colorectal cancers
S E Hiscox1, M B Hallett, M C Puntis
1Department of Surgery, University of Wales College of Medicine, Heath Park, Cardiff, U.K.
Abstract:
The c-met proto-oncogene product is a receptor tyrosine kinase that mediates the effects of the multifunctional cytokine hepatocyte growth factor/scatter factor (HGF/SF). We have studied the expression of both the c-met receptor and HGF/SF at both the protein and message level in colorectal cancer tissues of varying disease stage. All of the tumors displayed an overexpression of the c-met mRNA compared to their normal tissue counterparts while 16 of 21 tissues (75%) displayed up-regulation of c-met protein. No HGF/SF mRNA or protein could be detected in either tissue type. Viable tumor cells extracted from cancer tissue exhibited increased motility in response to HGF/SF stimulation demonstrating that c-met was functionally active. No correlation between expression of c-met and tumor stage or degree of differentiation was observed. HGF/SF is known to be a potent stimulator of tumor cell motility and invasion, two cellular properties essential for the metastatic development of cancers. The overexpression of the HGF/SF receptor in colorectal cancers may result in an increased sensitivity to HGF/SF, which may confer an enhanced metastatic potential to the cancer cells within the tumor body.
Insights
Colorectal cancer tissues overexpress the c-met receptor, a key protein in cell movement. This suggests increased sensitivity to hepatocyte growth factor/scatter factor (HGF/SF), potentially enhancing cancer metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The c-met proto-oncogene product is a receptor tyrosine kinase.
- It mediates the effects of hepatocyte growth factor/scatter factor (HGF/SF).
- HGF/SF is crucial for tumor cell motility and invasion, key factors in cancer metastasis.
Purpose of the Study:
- To investigate the expression of the c-met receptor and HGF/SF in colorectal cancer tissues.
- To assess the functional activity of c-met in colorectal cancer cells.
- To explore the correlation between c-met expression and clinicopathological features.
Main Methods:
- Studied c-met and HGF/SF expression at both mRNA and protein levels in colorectal cancer tissues.
- Utilized viable tumor cell extraction and stimulation assays.
- Analyzed expression data against tumor stage and differentiation grade.
Main Results:
- All tumors showed overexpression of c-met mRNA compared to normal tissues.
- 75% of colorectal cancer tissues displayed up-regulated c-met protein.
- No HGF/SF mRNA or protein was detected in either tumor or normal tissues.
- Stimulated tumor cells exhibited increased motility in response to HGF/SF, confirming functional c-met activity.
- No correlation was found between c-met expression and tumor stage or differentiation.
Conclusions:
- Colorectal cancers frequently overexpress the c-met receptor.
- This overexpression may lead to heightened sensitivity to HGF/SF.
- Such sensitivity could potentially enhance the metastatic potential of colorectal cancer cells.
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