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Enhancement of metastatic properties of pancreatic cancer cells by MUC1 gene encoding an anti‐adhesion molecule
Author(s) -
Satoh Shuji,
Hinoda Yuji,
Hayashi Toshiaki,
Burdick Michael D.,
Imai Kohzoh,
Hollingsworth Michael A.
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001115)88:4<507::aid-ijc1>3.0.co;2-0
Subject(s) - muc1 , pancreatic cancer , mucin , cancer research , in vitro , metastasis , cell adhesion molecule , laminin , biology , motility , cell culture , in vivo , microbiology and biotechnology , pathology , extracellular matrix , cancer , immunology , medicine , biochemistry , genetics
MUC1 mucin expression has been shown to be associated clinicopathologically with metastasis and poor clinical outcome in a variety of tumors. To further investigate this finding experimentally, human pancreatic cancer S2‐013 cells overexpressing MUC1 were used for spontaneous metastatic potential in nude mice. It was found that the number of lung metastases of MUC1 transfectants was significantly higher than that of control cells. To analyze the molecular mechanisms that underlie the increased metastatic activity, in vitro adhesion assays were performed. MUC1 mucin expression enhanced in vitro invasiveness and motility of S2‐013 cells, and decreased the binding of S2‐013 cells to type I collagen, Type IV collagen and laminin. Similar effects were not observed for cells expressing tandem repeat‐deleted MUC1 cDNA. Adhesion properties were abolished by benzyl‐α‐GalNAc treatment, indicating that glycosylation of the extracellular domain of MUC1 was essential for these biological adhesive functions. Our data support the hypothesis that MUC1 expression contributes to the metastatic ability of pancreatic cancer cells. Int. J. Cancer 88:507–518, 2000. © 2000 Wiley‐Liss, Inc.