Grignani G, Pacchiarini L, Almasio P, Pagliarino M, Gamba G, Rizzo S C, Ascari E
Int J Cancer. 1986 Aug 15;38(2):237-44. doi: 10.1002/ijc.2910380214.
We studied the mechanisms of platelet activation by sublines exhibiting different metastatic potential of two murine experimental tumors: sublines M4 and M9 of the benzopyrene-induced mFS6 sarcoma and sublines B77-AA6 and B77-3T3 of RSV-transformed BALB/c 3T3 fibroblasts. The neoplastic cells of both models induced platelet aggregation, secretion and prostaglandin biosynthesis. In the first model but not in the second, all these processes correlated with the in vivo malignancy of cells. Pretreatment of B77-AA6 and B77-3T3 cells with apyrase significantly decreased platelet aggregation, while pretreatment of M4 cells was ineffective. However, pretreatment with trypsin or neuraminidase was effective in reducing platelet aggregation induced by M4 cells, but not that induced by any of the others; furthermore, phospholipase A2 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 in vivo metastatic behavior.
苯并芘诱导的mFS6肉瘤的亚系M4和M9，以及劳氏肉瘤病毒转化的BALB/c 3T3成纤维细胞的亚系B77 - AA6和B77 - 3T3。两种模型的肿瘤细胞均能诱导血小板聚集、分泌和前列腺素生物合成。在第一个模型中，所有这些过程都与细胞的体内恶性程度相关，但在第二个模型中并非如此。用腺苷三磷酸双磷酸酶预处理B77 - AA6和B77 - 3T3细胞可显著降低血小板聚集，而预处理M4细胞则无效。然而，用胰蛋白酶或神经氨酸酶预处理可有效降低M4细胞诱导的血小板聚集，但对其他任何细胞系诱导的血小板聚集均无效；此外，磷脂酶A2可降低所有亚系的血小板反应。最后，在培养基离心后的沉淀中也发现了血小板激活活性。这些结果表明，癌细胞通过不同机制刺激血小板；通过细胞膜的唾液酸脂蛋白复合物激活血小板是肿瘤细胞的血小板聚集活性与其体内转移行为相关的模型所特有的。
