Cavanaugh P G, Sloane B F, Honn K V
Department of Biological Sciences, Wayne State University, Detroit, Mich.
Haemostasis. 1988;18(1):37-46. doi: 10.1159/000215781.
The ability of tumor cells to initiate coagulation and subsequent platelet aggregation is believed to facilitate the metastatic process. The mechanism by which tumor cells initiate thrombotic alterations is unclear. We have purified a plasma membrane protein platelet aggregating activity/procoagulant activity (PAA/PCA) from several rodent tumors which initiates the coagulation of homologous plasma and aggregation of homologous platelets by a mechanism independent of factor VII. This protein does not possess any proteinase activity; however, its activity is dependent upon the presence of factor X. In addition, PAA/PCA requires reconstitution with phospholipid for expression of activity. These results suggest that tumor cells express a unique protein which possesses procoagulant activity resulting in thrombin generation. Thrombin is responsible for subsequent tumor-cell-induced platelet aggregation.
肿瘤细胞引发凝血及随后血小板聚集的能力被认为有助于转移过程。肿瘤细胞引发血栓形成改变的机制尚不清楚。我们已从几种啮齿动物肿瘤中纯化出一种质膜蛋白,即血小板聚集活性/促凝血活性(PAA/PCA),它通过一种不依赖于因子VII的机制引发同源血浆的凝血和同源血小板的聚集。这种蛋白不具备任何蛋白酶活性;然而,其活性依赖于因子X的存在。此外,PAA/PCA需要与磷脂重构以表达活性。这些结果表明,肿瘤细胞表达一种具有促凝血活性的独特蛋白,导致凝血酶生成。凝血酶负责随后肿瘤细胞诱导的血小板聚集。