Reijerkerk A, Meijers J C M, Havik S R, Bouma B N, Voest E E, Gebbink M F B G
Department of Medical Oncology, University Medical Center Utrecht, Utrecht, The Netherlands.
J Thromb Haemost. 2004 May;2(5):769-79. doi: 10.1111/j.1538-7836.2004.00682.x.
Many studies have indicated that the plasminogen activation system may have a prominent role in cancer. Activation of the zymogen plasminogen into the serine protease plasmin by plasminogen activator is mediated by carboxyterminal basic amino acids in fibrin, including lysines and arginines. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a circulating carboxypeptidase B-type proenzyme that, after activation, removes carboxyterminal lysine or arginine residues in fibrin, resulting in decreased plasminogen activation and attenuated fibrinolysis. To determine directly whether TAFI is involved in primary tumor growth and metastasis formation, we examined the effects of TAFI deficiency on subcutaneous growth and experimentally or spontaneously induced pulmonary metastasis formation of different tumor cell types in mice. In all tumor models TAFI deficiency did not affect the formation and growth of primary and metastasized tumors.
许多研究表明，纤溶酶原激活系统可能在癌症中发挥重要作用。纤溶酶原激活剂将酶原纤溶酶原激活为丝氨酸蛋白酶纤溶酶的过程是由纤维蛋白中的羧基末端碱性氨基酸介导的，包括赖氨酸和精氨酸。凝血酶激活的纤维蛋白溶解抑制剂（TAFI）是一种循环的羧肽酶B型酶原，激活后可去除纤维蛋白中的羧基末端赖氨酸或精氨酸残基，导致纤溶酶原激活减少和纤维蛋白溶解减弱。为了直接确定TAFI是否参与原发性肿瘤生长和转移形成，我们研究了TAFI缺陷对小鼠不同肿瘤细胞类型皮下生长以及实验性或自发性诱导的肺转移形成的影响。在所有肿瘤模型中，TAFI缺陷均不影响原发性肿瘤和转移性肿瘤的形成与生长。
