The roles of adhesion molecule and cytokine in cancer metastasis

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1)B 16 mouse melanoma cells were much more adhered to vascular to vascular endothelial cells stimulated by interleukin-1 (IL-1). Since the adhesion was inhibited by antiintegrin a4 subunit antibody or vascular cell adhesion-1 (VCAM-1), integrin a4b1 on B16 cells was supposed to be interacted with VCAM-1 on endothelial cells. The effect of IL-1 was examined in lung metastasis of B 16 cells in mouse. Pretreatment of IL-1 increased lung metastasis more frequently and the lung metastasis was blocked by anti-a4 antibody. Together with the in vitro results, pretreatment of IL-1 induced VCAM-1 on endothelial cells and potentiated lung metastasis of B 16 cells expressing a4b1.2)The roles of adhesion molecule and cytokine were examined in organ specific metastasis. MAG cells, established from pleural effusion of the patient with esophageal cancer, were inoculated into foot pad, tail vein, or spleen of the nude mice. Metastases in the lymph node, lung, or liver were observed respectively. When cultured cells from metastatic foci were reinjected, each metastasis was observed more quickly. High metastatic cells were established respectively to lymph node, lung or liver after the procedures were performed 5 times. Growth rate, adhesion to extracellular matrix, cell migration, cell invasion to Matrigel, expression of integrin molecules and secretion of cytokine were examined in these high metastatic cells. As a result, each high metastatic cell decreased growth rate but increased cell adhesion, migration and invasion significantly. These changes were associated with expression of integrin on cells and secretion of cytokine.These data suggested expression of integrin molecules and secretion of cytokine play some roles in cancer metastasis and organ specific metastasis.