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A more recent version of this article appeared on June 1, 2006
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Submitted on November 14, 2005
Revised on March 9, 2006
Accepted on March 20, 2006
3
1 and 64 Integrin-dependent Tumor Cell Functions on Laminin-5
*University of Iowa, Department of Biological Sciences, Iowa City, IA 52240; School of Biomedical Sciences, Medical Sciences Building, University of Newcastle, Callaghan NSW 2308, Australia
Monitoring Editor: Mark Ginsberg
The basement membrane protein laminin-5 supports tumor cell adhesion and motility and is implicated at multiple steps of the metastatic cascade. Tetraspanin CD151 engages in lateral, cell surface complexes with both of the major laminin-5 receptors, integrins 
3
1 and 64. To determine the role of CD151 in tumor cell responses to laminin-5, we used retroviral RNA interference to efficiently silence CD151 expression in epidermal carcinoma cells. Near total loss of CD151 had no effect on steady state cell surface expression of 31, 64, or other integrins with which CD151 associates. However, CD151-silenced carcinoma cells displayed markedly impaired motility on laminin-5, accompanied by unusually persistent lateral and trailing edge adhesive contacts. CD151 silencing disrupted 31 integrin association with tetraspanin-enriched microdomains, reduced the bulk detergent extractability of 31, and impaired 31 internalization in cells migrating on laminin-5. Both 31-dependent and 64-dependent cell adhesion to laminin-5 were also impaired in CD151-silenced cells. Reexpressing CD151 in CD151-silenced cells reversed the adhesion and motility defects. Finally, loss of CD151 also impaired migration but not adhesion on substrates other than laminin-5. These data show that CD151 plays a critical role in tumor cell responses to laminin-5 and reveal promotion of integrin recycling as a novel potential mechanism whereby CD151 regulates tumor cell migration.
These authors contributed equally to this study.
Address correspondence to:
Christopher S. Stipp (christopher-stipp{at}uiowa.edu)
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