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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Increased fibronectin-receptor expression in colon carcinoma-derived HT 29 cells decreases tumorigenicity in nude mice.

BACKGROUND/AIMS: Following malignant transformation, epithelial cells of colorectal carcinomas, unlike normal colonic epithelial cells, no longer express the alpha 5 beta 1 fibronectin receptor. We hypothesized that the loss of alpha 5 beta 1 expression might facilitate the tumorigenicity of transformed colonic cells. METHODS: To examine this hypothesis, we established subclones of the human colon adenocarcinoma cell line HT 29, which differ in their fibronectin receptor expression and tested their tumorigenicity in nude mice. RESULTS: Our data indicate that the capacity to form tumors in nude mice after subcutaneous injection was significantly lower for alpha 5-positive than for alpha 5-negative cell clones. In addition, tumors from clones expressing no detectable levels of alpha 5 beta 1 grew rapidly, whereas tumors expressing elevated levels of fibronectin receptor grew slowly. Despite similar rates of adhesion to fibronectin for alpha 5-positive and alpha 5-negative cell clones in vitro, deposition of fibronectin in tumor-surrounding stroma was increased in tumors derived from alpha 5-positive cells. CONCLUSIONS: Our results indicate that an increase of the alpha 5 beta 1- mediated interaction of malignant cells with the extracellular matrix may be responsible for decreased tumorigenicity of malignant transformed cells in colorectal carcinomas.[1]

References

  1. Increased fibronectin-receptor expression in colon carcinoma-derived HT 29 cells decreases tumorigenicity in nude mice. Stallmach, A., von Lampe, B., Orzechowski, H.D., Matthes, H., Riecken, E.O. Gastroenterology (1994) [Pubmed]
 
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