title: Reduction of syndecan-1 expression in differentiated type early gastric cancer and background mucosa with gastric cellular phenotype.
abstract: BACKGROUND
  Syndecan-1 is known to play a role as a cell adhesion molecule, similar to E-cadherin, and is associated with the maintenance of epithelial morphology. The purpose of this study was to elucidate the role and alterations of syndecan-1 expression in comparison with those of E-cadherin in different cellular phenotypes of differentiated-type gastric cancers (DGCs).
  
  
  METHODS
  A total of 80 DGCs at an early stage, and their adjacent mucosa, were evaluated by both immunohistochemistry and in situ hybridization. Syndecan-1 and E-cadherin were assessed by immunohistochemical staining with an anti-syndecan-1 and an anti-E-cadherin antibody, respectively. Based on immunohistochemistry, DGCs and their surrounding mucosa were divided into four types: gastric type (G-type), ordinary type (O-type), complete-intestinal type (CI-type), and null type.
  
  
  RESULTS
  The expression sites of syndecan-1 mRNA mostly coincided with those of syndecan-1 protein. Syndecan-1 expression was significantly lower in G-type cancers (30%) than in O- (81%) and CI-type cancers (92%) ( P = 0.0001 and P = 0.004, respectively), but E-cadherin did not show this result. In addition, syndecan-1 expression was significantly reduced in DGCs comprised partly of poorly differentiated adenocarcinoma or signet-ring cell carcinoma, compared to DGCs demonstrating papillary and/or tubular adenocarcinoma ( P = 0.02). G-type intestinal metaplasia (IM) surrounding the tumors was observed in 21% of G-type cancers, in 0% of O-, and in 10% of CI-type cancers ( P = 0.01; G-type vs O-type). Reduction of syndecan-1 expression was significant in G-type IM (25%) compared to non-G-type IM (75%; P = 0.02).
  
  
  CONCLUSIONS
  Syndecan-1 plays a role in the growth of G-type cancers at an early stage compared with E-cadherin changes, and the reduction of syndecan-1 expression in IM surrounding the tumors may influence the growth of G-type cancer.
authors.affiliation: Third Department of Internal Medicine, Asahikawa Medical College, 2-1-1-1 Midorigaoka-Higashi, 078-8510, Asahikawa, Japan.
authors.forename: Jiro
authors.initials: J
authors.lastname: Watari
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Saitoh
authors.forename: Mikihiro
authors.initials: M
authors.lastname: Fujiya
authors.forename: Naomi
authors.initials: N
authors.lastname: Shibata
authors.forename: Hiroki
authors.initials: H
authors.lastname: Tanabe
authors.forename: Yuhei
authors.initials: Y
authors.lastname: Inaba
authors.forename: Kotaro
authors.initials: K
authors.lastname: Okamoto
authors.forename: Atsuo
authors.initials: A
authors.lastname: Maemoto
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Ohta
authors.forename: Atsumi
authors.initials: A
authors.lastname: Yasuda
authors.forename: Tokiyoshi
authors.initials: T
authors.lastname: Ayabe
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Ashida
authors.forename: Kinichi
authors.initials: K
authors.lastname: Yokota
authors.forename: Takeshi
authors.initials: T
authors.lastname: Obara
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kohgo
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D015820:Cadherins / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008562:Membrane Glycoproteins / Q000378:metabolism*; D010641:Phenotype; D011509:Proteoglycans / Q000378:metabolism*; D013274:Stomach Neoplasms / Q000378:metabolism* / Q000473:pathology; D053668:Syndecan-1; D053667:Syndecans
chemical_list: D015820:Cadherins; D008562:Membrane Glycoproteins; D011509:Proteoglycans; C508241:SDC1 protein, human; D053668:Syndecan-1; D053667:Syndecans