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J Korean Cancer Assoc > Volume 29(2); 1997 > Article
Journal of the Korean Cancer Association 1997;29(2): 309-320.
Role of Cell Surface Mucin on Invasion and Metastasis of HM7 Colon Cancer Cells
Wan Hee Yoon, Hae Duck Park, Kyu Lim, Byung Doo Hwang
1Department of Surgery, Chungnam National University, Taejon, Korea.
2Department of Biochemistry, School of Medicine, Chungnam National University, Taejon, Korea.
Mucinous colorectal cancers have a poorer prognosis than which colorectal cancer produce low amount of mucin, but the exact mechanism is not well understood. The present study was undertaken to elucidate the exact mechanism of invasion and metastasis of high mucin producing colon cancer cells using mucin glycosylation inhibitor, benzyl-alpha-N-acetylgalactosamine.
To evaluate the effect of glycosylated mucin on invasion and metastasis, in vitro invasion, metalloproteinases (MMPs) activity, cell-matrix protein binding, cell-cell aggregation, as well as endothelial leukocyte adhesion molecule (ELAM-1) binding and cell surface expression of various mucin related antigens were analyzed.
MMPs activity in conditioned medium and invasion of ECM-coated porous filters by benzyl-alpha-GalNAc treated HM7 cells were decreased. There was no difference between control and treated HM7 cells in terms of matrix protein binding assay, but treated HM7 cells showed higher homotypic cell adhesion. The binding activity of treated HM7 cells to ELAM-1 was significantly decreased and fixed cell binding of MoAb SNH-3, 19-9 (specific for sialyl-Lewis X and sialyl-Lewis A) were also significantly decreased.
These results suggest that glycosylated mucin modulates ELAM-1 binding, MMPs activity and homotypic cell adhesion, therefore enhance invasive and metastatic properties of human colon cancer cells.
Key words: Mucin;HM7 colon cancer cells;Benzyl-alpha-GalNAc;Invasion;Metastasis
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