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Annals of Surgical Oncology, Vol 4, Issue 4 361-368, Copyright © 1997 by Society of Surgical Oncology
ARTICLES |
S. Nakamori, H. Okamoto, T. Kusama, K. Shinkai, M. Mukai, H. Ohigashi, O. Ishikawa, H. Furukawa, S. Imaoka and H. Akedo
Department of Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases, Japan.
BACKGROUND: Tumor cells induce endothelial cell retraction before invasion. In pancreatic cancer cells, the factors affecting endothelial cell retraction are not well-understood. METHODS: The activities of the endothelial cell retraction in conditioned media (CM) derived from three human pancreatic cancer cell lines, PSN-1, MiaPaca-2, and Capan-1, were measured for the amount of intercellular junctional transport of FITC dextran through an endothelial cell monolayer in a transwell cell culture system. RESULTS: The CM derived from the three pancreatic cancer cells induced endothelial cell retraction. The endothelial cell retraction activity in the CM from PSN-1 cells was significantly higher than those from MiaPaca-2 and Capan-1 cells. The CM from PSN-1 cells enhanced both the adhesion and the invasion of MiaPaca-2 and Capan-1 cells. The factors with endothelial cell retraction activity in the CM from PSN-1 cells were characterized as heat-stable, trypsin-sensitive glycoproteins ranging from 10,000 to 50,000 in molecular weight, and were found both in heparin-bound and unbound fractions. CONCLUSIONS: PSN-1 cells produced and secreted at least two factors inducing the endothelial cell retraction. The factors could play an important role in the establishment of invasion and metastasis of PSN-1 cells.
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