Reduction of syndecan-1 expression in differentiated type early gastric cancer and background mucosa with gastric cellular phenotype.
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.
Watari
Jiro
J
Third Department of Internal Medicine, Asahikawa Medical College, 2-1-1-1 Midorigaoka-Higashi, 078-8510, Asahikawa, Japan.
Saitoh
Yusuke
Y
Fujiya
Mikihiro
M
Shibata
Naomi
N
Tanabe
Hiroki
H
Inaba
Yuhei
Y
Okamoto
Kotaro
K
Maemoto
Atsuo
A
Ohta
Tomoyuki
T
Yasuda
Atsumi
A
Ayabe
Tokiyoshi
T
Ashida
Toshifumi
T
Yokota
Kinichi
K
Obara
Takeshi
T
Kohgo
Yutaka
Y
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
D015820:Cadherins; D008562:Membrane Glycoproteins; D011509:Proteoglycans; C508241:SDC1 protein, human; D053668:Syndecan-1; D053667:Syndecans