Premium
Expression of the urokinase receptor regulates focal adhesion assembly and cell migration in adenoid cystic carcinoma cells
Author(s) -
AbuAli Samah,
Sugiura Tsuyoshi,
Takahashi Miho,
Shiratsuchi Toru,
Ikari Tatsuya,
Seki Katsuhiro,
Hiraki Akimitsu,
Matsuki Ryousuke,
Shirasuna Kanemitsu
Publication year - 2005
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20242
Subject(s) - adenoid cystic carcinoma , focal adhesion , cancer research , receptor , microbiology and biotechnology , urokinase receptor , urokinase , adhesion , cell migration , chemistry , cell , carcinoma , biology , pathology , medicine , signal transduction , biochemistry , organic chemistry
Adenoid cystic carcinoma (AdCC) cell lines (ACCS and ACCT) showed higher migration responses and adhesion to the extracellular matrix (ECM), especially types I and IV collagen, than did the oral squamous cell carcinoma (SCC) lines (NA and TF). The response to collagens was largely and exclusively inhibited by anti‐α 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, an 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 α 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. © 2004 Wiley‐Liss, Inc.