Polymorphic expression of decay‐accelerating factor in human colorectal cancer
- 1 February 2001
- journal article
- Published by Wiley in Journal of Gastroenterology and Hepatology
- Vol. 16 (2) , 184-189
- https://doi.org/10.1046/j.1440-1746.2001.02418.x
Abstract
Background: We have previously shown that expression of decay‐accelerating factor (DAF), a complement regulatory protein, is enhanced immunohistochemically on the luminal surface of cancer glands in human colorectal cancer and is detected in stool specimens of patients with colorectal cancer. The amount of DAF present in the stools might be influenced by the stability of DAF on the cell surface which is regulated by biochemical properties such as glycosylation of the protein. In the present study, to help elucidate the mechanism for the release of DAF from human colorectal cancers, we biochemically analyzed DAF expression by western and northern blotting by using surgically resected specimens of colorectal cancers. Methods: Surgically resected colorectal cancer tissues were obtained from 10 patients. Expression of DAF was determined by western and northern blotting, and glycosylation of DAF protein was analyzed with glycosidase digestion. Results: Northern blot analysis demonstrated that the expression of DAF mRNA in colorectal cancer was enhanced two‐ to threefold compared with normal tissues. In western blotting, expression of DAF protein in the cancer tissue was increased, and heterogeneity in the apparent molecular weight of DAF was observed among patients. When o‐linked sugars were removed, this heterogeneity of DAF size diminished. Conclusions: The polymorphic expression of DAF in colorectal cancer is likely to reflect variability in the o‐glycosylation of the protein. We speculate that this variability could affect the stability of DAF on the surfaces of cancer cells and, in turn, the amount of DAF shed into the stools of colorectal cancer patients.Keywords
This publication has 24 references indexed in Scilit:
- Expression and regulation by interferon-γ of the membrane-bound complement regulators CD46 (MCP), CD55 (DAF) and CD59 in gastrointestinal tumoursEuropean Journal Of Cancer, 1999
- Comparison of O-Linked Carbohydrate Chains in MUC-1 Mucin from Normal Breast Epithelial Cell Lines and Breast Carcinoma Cell Lines:Journal of Biological Chemistry, 1996
- Interleukin 4 acts as an inducer of decay-accelerating factor gene expression in human intestinal epithelial cellsGastroenterology, 1996
- A family of UDP-GalNAc: polypeptide N-acetylgalactosaminyl-transferases control the initiation of mucin-type O-linked glycosylationGlycobiology, 1996
- Detection of decay-accelerating factor in stool specimens of patients with colorectal cancerGastroenterology, 1995
- Complement-mediated tumor cell damage induced by antibodies against membrane cofactor protein (MCP, CD46).The Journal of Experimental Medicine, 1990
- Decay-Accelerating Factor: Biochemistry, Molecular Biology, and FunctionAnnual Review of Immunology, 1989
- The mechanism of action of decay-accelerating factor (DAF). DAF inhibits the assembly of C3 convertases by dissociating C2a and Bb.The Journal of Experimental Medicine, 1987
- Cloning of decay-accelerating factor suggests novel use of splicing to generate two proteinsNature, 1987
- Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4Nature, 1970