Expression of the urokinase receptor regulates focal adhesion assembly and cell migration in adenoid cystic carcinoma cells
Expression of the urokinase receptor regulates focal adhesion assembly and cell migration in adenoid cystic carcinoma cells
复制标题
DOI：
10.1002/jcp.20242
复制
发表时间：
2005-05-01
影响因子：
5.6
通讯作者：
Shirasuna, K
中科院分区：
文献类型：
--
作者：
Abu-Ali, S;Sugiura, T;Shirasuna, K
腺样囊性癌 (AdCC) 细胞系（ACCS 和 ACCT）比口腔鳞状细胞癌 (SCC) 细胞系（NA 和 TF）表现出更高的迁移反应和对细胞外基质 (ECM)（尤其是 I 型和 IV 型胶原）的粘附。对胶原的反应在很大程度上且完全被抗α(2)(2整联蛋白抗体抑制。此外，AdCC细胞系比SCC细胞系表达更高水平的尿激酶型纤溶酶原激活剂受体(uPAR)。当AdCC细胞铺在胶原上时，uPAR的表面水平增加，并且组装了许多由uPAR、纽蛋白和桩蛋白组成的粘着斑；而胶原刺激的SCC细胞对应物或AdCC铺在其他类型的 ECM（例如纤连蛋白）上的细胞无法组装这种明确的粘着斑，为了阐明 uPAR 与胶原诱导事件的关联，建立了用表达反义 uPAR RNA 的载体转染的所有 ACCS-AS 细胞系，并显示 uPAR 减少（在蛋白质和 mRNA 水平上约为亲代 ACCS 的 10%）。 α(2) 整合素、纽蛋白和桩蛋白。这些发现表明，由于 uPAR 的过度表达，AdCC 具有迁移到 I 型和 IV 型胶原的倾向，这在粘着斑组装和迁移中发挥着关键作用 (c) 2004 Wiley-Liss, Inc.。
Adenoid cystic carcinoma (AdCC)cell lines (ACCS and ACCT) showed higher migration responses and adhesion to the extracellular matrix (ECM), especially types I and IVcollagen, than did the oral squamous cell carcinoma (SCC) lines (NA and TF). The response to collagens was largely and exclusively inhibited by anti-alpha(2)(2 integrin antibody. Moreover, AdCC cell lines expressed higher surface levels Of urokinase-type plasminogen activator receptor (uPAR) than did SCC cell lines. When AdCC cells were plated on collagen, the surface level Of uPAR was increased, and numerous focal adhesions consisting of uPAR, vinculin, and paxillin were assembled; whereas collagen-stimulated SCC cell Counterparts or AdCC cells plated on other types of ECM, Such as fibronectin, failed to assemble such definite focal adhesions. In order to elucidate the association Of uPAR with collagen-induced events, all ACCS-AS cell line transfected with a vector expressing antisense uPAR RNA was established and shown to have reduced uPAR (about 10% that of parental ACCS at both the protein and mRNA levels). ACCS-AS showed a strong reduction of collagen-stimulated migration and focal adhesion assembly of alpha(2) integrin, vinculin, and paxillin. These findings suggest that AdCC has a proclivity for migrating to types I and IV collagens due to the overexpression of uPAR, which plays a key role in focal adhesion assembly and migration. (c) 2004 Wiley-Liss, Inc.