Interaction Of Platelets And Tumor Cells: Differentiation Between Nine Human Tumor Cell Lines Based On Aggregation And Effects Of Apyrase, Hirudin And Phospholipase D

Aggregation mechanisms have been examined in a homologous system using heparinized human platelet-rich plasma with cell lines derived from human tumors. The A549 (epithelial lung carcinoma) and Hut23 (adenocarcinoma) did not aggregate platelets at 10⁷ cells/ml. Other cell lines could not be classified by aggregation pattern alone since all gave biphasic or quasibiphasic patterns. HT 29 (adenocarcinoma) , SKBR3 (adenocarcinoma), HT 144 (melanoma) and Hut 20 (large cell lung carcinoma) were inhibited by apyrase and phospholipase D but not by hirudin: aggregation induced by this group is probably primarily dependent on ADP. Aggregation by SKNMC (mesothelioma) and Hut 28 (mesothelioma) was inhibited by hirudin and phospholipase D but not by apyrase. Aggregation by this second group probably involves activation of the clotting system in the early stages but can be differentiated from a similar mechanism with U87MG since thq latter is not inhibited by phospholipase D. Phospholipase C had no effect on any cell line and phospholipase A2 inhibited all cell lines, as did its hydrolytic product, lysolecthin. Platelet aggregating material (PAM) could not be isolated by urea extraction of any of these human tumor cells. These results suggest that various inhibitors are necessary to allow classification of mechanisms of tumor cell-induced platelet aggregation.