Characterization of platelet aggregation induced by the human melanoma cell line HMV-I: roles of heparin, plasma adhesive proteins, and tumor cell membrane proteins.

Abstract

We investigated the in vitro mechanism of platelet aggregation induced by HMV-I human melanoma cells. HMV-I cells, in the absence of exogenous plasma proteins, induced platelet aggregation, followed by the release reaction. Heparin at an anticoagulant concentration had no effect on the aggregation. Calcium ion was essential for this tumor cell-platelet interaction and could not be replaced by magnesium. Among the adhesive proteins containing RGD sequences that have been reported to enhance experimental metastasis, fibrinogen and thrombospondin significantly enhanced the aggregation induced by HMV-I cells, fibronectin and von Willebrand factor inhibited it, and vitronectin had no effect. To identify the platelet-aggregating factor(s) of the tumor cells, we have developed a monoclonal antibody against HMV-I cells that can inhibit HMV-I cell-induced platelet aggregation. Immunoprecipitation analysis revealed that this antibody recognized an Mr 71,000 membrane protein. These results suggest that the association between the tumor cells and platelets is mediated by the Mr 71,000 membrane protein recognized by this monoclonal antibody.