Paxillin modulates squamous cancer cell adhesion and is important in pressure-augmented adhesion

Conway, William C., Van der Voort van Zyp, Jochem, Thamilselvan, Vijayalakshmi, Walsh, Mary F., Crowe, David L. and Basson, Marc D. (2006) Paxillin modulates squamous cancer cell adhesion and is important in pressure-augmented adhesion. Journal of Cellular Biochemistry, 98 6: 1507-1516. doi:10.1002/jcb.20819


Author Conway, William C.
Van der Voort van Zyp, Jochem
Thamilselvan, Vijayalakshmi
Walsh, Mary F.
Crowe, David L.
Basson, Marc D.
Title Paxillin modulates squamous cancer cell adhesion and is important in pressure-augmented adhesion
Journal name Journal of Cellular Biochemistry   Check publisher's open access policy
ISSN 0730-2312
1097-4644
Publication date 2006-08-15
Sub-type Article (original research)
DOI 10.1002/jcb.20819
Volume 98
Issue 6
Start page 1507
End page 1516
Total pages 10
Place of publication Hoboken, NJ, United States
Publisher John Wiley & Sons
Language eng
Abstract Paxillin is an adapter protein regulating signaling and focal adhesion assembly that has been linked to malignant potential in many malignancies. Overexpression of paxillin has been noted in aggressive tumors. Integrin-mediated binding through the focal adhesion complex is important in metastatic adhesion and is upregulated by extracellular pressure in malignant colonocytes through FAK and Src activation. Neither head and neck cancers nor paxillin have been studied in this regard. We hypothesized that paxillin would play a role in modulating squamous cancer adhesion both at baseline and under conditions of increased extracellular pressure. Using SCC25 tongue squamous cancer cells stably transfected with either an empty selection vector or paxillin expression and selection vectors, we studied adhesion to collagen, paxillin, FAK, and Src expression and phosphorylation in cells maintained for 30 min under ambient or 15 mmHg increased pressure conditions. Paxillin-overexpressing cells exhibited adhesion 121 ± 2.9% of that observed in vector-only cells (n = 6, P < 0.001) under ambient pressure. Paxillin-overexpression reduced FAK phosphorylation. Pressure stimulated adhesion to 118 ± 2.3% (n = 6, P  < 0.001) of baseline in vector-only cells, similar to its effect in the parental line, and induced paxillin, FAK, and Src phosphorylation. However, increased pressure did not stimulate adhesion or phosphorylate paxillin, FAK, or Src further in paxillin-overexpressing cells. Metastasizing squamous cancer cell adhesiveness may be increased by paxillin-overexpression or by paxillin activation by extracellular pressure during surgical manipulation or growth within a constraining compartment. Targeting paxillin in patients with malignancy and minimal tumor manipulation during surgical resection may be important therapeutic adjuncts.
Keyword Adhesion
Cancer
FAK
Matrix
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 25 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 29 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Mon, 14 Mar 2011, 18:52:29 EST