Alonso D F, De Lorenzo M S, Tejera A M, Gomez D E
Department of Science and Technology, Quilmes National University, Buenos Aires, 1876, Argentina.
Oncol Rep. 1998 Jan-Feb;5(1):209-12.
We have examined the relationship between the procoagulant activity of F3II mouse mammary carcinoma cells and the production of urokinase, a profibrinolytic serine protease involved in tumor invasion and hematogenous metastasis. F3II cells were capable of inducing the conversion of purified fibrinogen to fibrin in the presence of calcium and plasma traces. Immunocytochemical examination of semi-confluent monolayers demonstrated that F3II cells also synthesized high levels of urokinase. Although fibrinogen did not modify profibrinolytic activity produced by F3II monolayers, fibrin formation increased tumor-derived urokinase activity by two-fold. The present data provide new insights into the cooperative role of coagulation and fibrinolysis facilitating and perpetuating tumor invasion.
我们研究了F3II小鼠乳腺癌细胞的促凝血活性与尿激酶产生之间的关系，尿激酶是一种参与肿瘤侵袭和血行转移的纤维蛋白溶解丝氨酸蛋白酶。F3II细胞在存在钙和微量血浆的情况下能够诱导纯化的纤维蛋白原转化为纤维蛋白。对半汇合单层细胞的免疫细胞化学检查表明，F3II细胞也合成高水平的尿激酶。尽管纤维蛋白原不会改变F3II单层细胞产生的纤维蛋白溶解活性，但纤维蛋白的形成使肿瘤来源的尿激酶活性增加了两倍。目前的数据为凝血和纤维蛋白溶解在促进和维持肿瘤侵袭中的协同作用提供了新的见解。
