Description:
<jats:title>Abstract</jats:title><jats:p>We studied the mechanisms of platelet activation by sublines exhibiting different metastatic potential of two murine experimental tumors: sublines M<jats:sub>4</jats:sub> and M<jats:sub>9</jats:sub> of the benzopyrene‐induced mFS6 sarcoma and sub‐ lines B77‐AA6 and B77–3T3 of RSV‐transformed BALB/c 3T3 fibroblasts. The neoplastic cells of both models induced platelet aggregation, secretion and prosta‐glandin biosynthesis. In the first model but not in the second, all these processes correlated with the <jats:italic>in vivo</jats:italic> malignancy of cells. Pretreatment of B77‐AA6 and B77–3T3 cells with apyrase significantly decreased platelet aggregation, while pretreatment of M<jats:sub>4</jats:sub> cells was ineffective. However, pretreatment with trypsin or neuraminidase was effective in reducing platelet aggregation induced by M<jats:sub>4</jats:sub> cells, but not that induced by any of the others; furthermore, phospholipase A<jats:sub>2</jats:sub> reduced the platelet response by all sublines. Finally, platelet‐activating activity was also found in the pellets obtained following centrifugation of culture media. These results suggest that platelets are stimulated by cancer cells through different mechanisms; platelet activation by a sialo‐lipo‐protein complex of the cellular membrane was found to be characteristic of the model in which the platelet‐aggregating activity of neoplastic cells correlated with their <jats:italic>in vivo</jats:italic> metastatic behavior.</jats:p>