Bajou K, Noël A, Gerard R D, Masson V, Brunner N, Holst-Hansen C, Skobe M, Fusenig N E, Carmeliet P, Collen D, Foidart J M
Laboratory of Tumor and Developmental Biology, University of Liège, Belgium.
Nat Med. 1998 Aug;4(8):923-8. doi: 10.1038/nm0898-923.
Acquisition of invasive/metastatic potential through protease expression is an essential event in tumor progression. High levels of components of the plasminogen activation system, including urokinase, but paradoxically also its inhibitor, plasminogen activator inhibitor 1 (PAI1), have been correlated with a poor prognosis for some cancers. We report here that deficient PAI1 expression in host mice prevented local invasion and tumor vascularization of transplanted malignant keratinocytes. When this PAI1 deficiency was circumvented by intravenous injection of a replication-defective adenoviral vector expressing human PAI1, invasion and associated angiogenesis were restored. This experimental evidence demonstrates that host-produced PAI is essential for cancer cell invasion and angiogenesis.
通过蛋白酶表达获得侵袭/转移潜能是肿瘤进展中的一个关键事件。纤溶酶原激活系统的多种成分,包括尿激酶,以及其抑制剂纤溶酶原激活物抑制剂1(PAI1),在某些癌症中,其高水平表达与不良预后相关,但存在矛盾的是,PAI1高水平表达也与不良预后相关。我们在此报告,宿主小鼠中PAI1表达缺陷可阻止移植的恶性角质形成细胞的局部侵袭和肿瘤血管生成。当通过静脉注射表达人PAI1的复制缺陷型腺病毒载体来克服这种PAI1缺陷时,侵袭和相关的血管生成得以恢复。这一实验证据表明,宿主产生的PAI对癌细胞侵袭和血管生成至关重要。