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Influence of Tumor-derived Interleukin 1 on Melanoma-Endothelial Cell Interactions in Vitro

Drug Targeting [F. J. B., P. E. T.] and Biology of Metastasis Laboratories [I. R. H., J. F. M.], Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX; Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London [D. O. H.]; and Division of Endocrinology, National Institute of Biological Standards and Control, Blanche Lane, South Mimms, Hertfordshire [S. S., S. P.], England

Human melanoma cell lines that express high constitutive levels of the metastasis-associated marker intercellular adhesion molecule 1 (ICAM-1) were found to secrete interleukin 1 (IL-1) in vitro. Experiments with neutralizing antibodies showed that this cytokine was responsible for their expression of ICAM-1 but not that of two other progression/metastasis markers, Muc-18 and Gp IIb/IIIa. The IL-1 present in melanoma-conditioned medium induced the expression of vascular cell adhesion molecule 1, endothelial-leukocyte adhesion molecule 1, and ICAM-1 on human umbilical vein endothelial cells (ECs) in culture and increased the rate at which melanoma cells and ECs adhered to each other. IL-1-producing melanoma lines adhered significantly more rapidly to ECs than did non-IL-1-producing lines, and this enhancement was reduced by prior incubation of the melanoma cells with neutralizing anti-IL-1 antibodies. Similarly, endothelial cells treated with conditioned medium from IL-1-producing melanoma lines adhered significantly more rapidly to melanoma cells than did ECs treated with medium from non-IL-1-producing melanoma lines, and this enhancement was abolished by addition of anti-IL-1 antibodies to EC cultures in conditioned medium. Blocking antibodies to endothelial vascular cell adhesion molecule 1, endothelial-leukocyte adhesion molecule 1, and ICAM-1 failed to inhibit melanoma-EC adhesion, but an antibody to tumor cell GpIIb/IIIa did block adhesion by up to 44%. The ability to secrete IL-1 could increase the metastatic potential of melanoma cells by stimulating tumor cell-EC adhesion.

¹ To whom requests for reprints should be addressed, at Cancer Immunobiology Center, Southwestern Medical School, University of Texas Health Science Center, 5323 Harry Hines Blvd., Dallas, TX 75235.

Received 11/30/90. Accepted 7/ 8/91.

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