PMID: 7525435Jul 1, 1994Paper

Molecular mechanism in hematogenous metastasis of pancreas carcinoma--possible implication of tumor-derived cytokine in a cell-to-cell interaction of pancreas carcinoma and vascular endothelial cells

[Hokkaido igaku zasshi] The Hokkaido journal of medical science
M Kaji

Abstract

Cellular adhesion between sialyl Lewis a (SLea)-positive pancreas carcinoma and endothelial cells is augmented by exogenous cytokines such as interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha through an upregulated E-selectin expression on endothelial cells. Preincubation of pancreas carcinoma cells with endothelial cells for 4-6 hours at the ratio of 1:10 induced E-selectin expression on endothelial cell surface, and dramatically increased subsequent attachment of SLea-positive pancreas carcinoma with endothelial cells. Paraformaldehyde-fixed PCI cells also induced E-selectin on vascular endothelial cells upon direct contact with endothelial cells. Culture supernatants from all six pancreas carcinoma cell lines contained soluble, E-selectin-inducible factors. Antibodies against SLea and E-selectin but not SLex or ICAM-1 blocked the increased pancreas carcinoma-to-endothelial attachment. These findings suggested that SLea-positive pancreas carcinoma cells produced E-selectin-inducing cytokines, both in the soluble and the membrane bound forms, resulted in augmented attachment to endothelial cells in vitro. The soluble factor lost its activity to induce E-selectin at 70 degrees C, and was different from IL-1-beta or ...Continue Reading

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