Tumor cell-platelet aggregation: induced by cathepsin B-like proteinase and inhibited by prostacyclin.
The ability of tumor cells to metastasize may be related to their ability to promote aggregation of host platelets. The use of inhibitors of cysteine proteinases resulted in parallel inhibition of B16 amelanotic melanoma-induced platelet aggregation and of a cathepsin B activity. The antimetastatic agent prostacyclin inhibited platelet aggregation induced by the tumor cells and by papain, a cathepsin B-mimicking agent.
D000818:Animals; D002401:Cathepsin B; D002403:Cathepsins / Q000378:metabolism*; D002478:Cells, Cultured; D003546:Cysteine Endopeptidases; D010450:Endopeptidases / Q000378:metabolism*; D011464:Epoprostenol / Q000494:pharmacology*; D006801:Humans; D008545:Melanoma / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009374:Neoplasms, Experimental / Q000378:metabolism; D010206:Papain / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D011480:Protease Inhibitors / Q000494:pharmacology
D011453:Prostaglandins; D011480:Protease Inhibitors; D011464:Epoprostenol; D002403:Cathepsins; D010450:Endopeptidases; D003546:Cysteine Endopeptidases; D002401:Cathepsin B; D010206:Papain