title: Polymorphic expression of decay-accelerating factor in human colorectal cancer.
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.
authors.affiliation: First Department of Internal Medicine, Okayama University Medical School, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: M
authors.initials: M
authors.lastname: Mizuno
authors.forename: M
authors.initials: M
authors.lastname: Kawada
authors.forename: T
authors.initials: T
authors.lastname: Uesu
authors.forename: J
authors.initials: J
authors.lastname: Nasu
authors.forename: K
authors.initials: K
authors.lastname: Takeuchi
authors.forename: H
authors.initials: H
authors.lastname: Okada
authors.forename: Y
authors.initials: Y
authors.lastname: Endo
authors.forename: T
authors.initials: T
authors.lastname: Fujita
authors.forename: T
authors.initials: T
authors.lastname: Tsuji
mesh_terms: D000328:Adult; D000368:Aged; D015152:Blotting, Northern; D015153:Blotting, Western; D018958:CD55 Antigens / Q000187:drug effects / Q000235:genetics*; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000628:therapy; D005260:Female; D006026:Glycoside Hydrolases / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D008970:Molecular Weight; D011110:Polymorphism, Genetic / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D018958:CD55 Antigens; D012333:RNA, Messenger; D006026:Glycoside Hydrolases