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omega-3 fatty acids decrease endothelial adhesion of human colorectal carcinoma cells.
M Kontogiannea1, A Gupta, F Ntanios
1Department of Surgery, Royal Victoria Hospital, Montreal, Quebec, Canada.
The Journal of Surgical Research
|July 18, 2000
Summary
Omega-3 fatty acids reduce colon cancer spread to the liver by decreasing cancer cell adhesion to liver cells. This may involve reducing the expression of a key adhesion molecule called sialyl-Lewis(x).
Area of Science:
- Oncology
- Molecular Biology
- Nutrition Science
Background:
- Diets rich in omega-3 fatty acids show promise in reducing colon cancer initiation and promotion.
- The impact of omega-3 fatty acids on the formation of hepatic metastases, a critical stage in cancer spread, is less understood.
- Cancer cell adhesion to hepatic endothelial cells is a key step in the metastatic cascade.
Purpose of the Study:
- To investigate the effect of omega-3 fatty acid enrichment on the adhesion of human colorectal carcinoma (HCRC) cells to hepatic endothelial cells.
- To explore the potential role of omega-3 fatty acids in preventing hepatic metastasis formation.
Main Methods:
- Human colorectal carcinoma (CX-1) cells were cultured in omega-3 fatty acid-enriched medium.
- Membrane fatty acid composition was analyzed using gas chromatography.
- Adhesion assays were performed using (51)Cr-labeled CX-1 cells and stimulated human umbilical vein and hepatic sinusoidal endothelial cells.
- Immunohistochemical analysis was conducted to assess the expression of sialyl-Lewis(x) on CX-1 cells.
Main Results:
- Gas chromatography confirmed significant enrichment of omega-3 fatty acids (docosahexanoic acid) in CX-1 cell membranes.
- Binding of CX-1 cells to both types of endothelial cells decreased significantly after omega-3 treatment (from 38.4% to 11.58%).
- Immunocytochemical analysis revealed a reduction in sialyl-Lewis(x) expression on omega-3 treated CX-1 cells.
Conclusions:
- Omega-3 fatty acids may offer protection against the development of hepatic metastases.
- The mechanism underlying this protective effect appears to be reduced endothelial cell adhesion.
- This reduction in adhesion may be attributed to decreased expression of the endothelial receptor sialyl-Lewis(x).