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A more recent version of this article appeared on March 1, 2007
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Submitted on March 6, 2006
Revised on December 4, 2006
Accepted on December 18, 2006
*Division of Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, United Kingdom; Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037
Monitoring Editor: Paul Forscher
Most sporadic colorectal tumors carry truncation mutations in the adenomatous polyposis coli (APC) gene. The APC protein is involved in many processes that govern gut tissue. In addition to its involvement in the regulation of 
-catenin, APC is a cytoskeletal regulator with direct and indirect effects on microtubules. Cancer-related truncation mutations lack direct and indirect binding sites for microtubules in APC, suggesting that loss of this function contributes to defects in APC-mutant cells. In this study we show that loss of APC results in disappearance of cellular protrusions and decreased cell migration. These changes are accompanied by a decrease in overall microtubule stability and also by a decrease in post translationally modified microtubules in the cell periphery particularly the migrating edge. Consistent with the ability of APC to affect cells shape, the over expression of APC in cells can induce cellular protrusions. These data demonstrate that cell migration and microtubule stability are linked to APC status thus revealing a weakness in APC-deficient cells with potential therapeutic implications.
Present address: Polyphor Ltd, Gewerbestrasse 14, CH-4123 Allschwil, Switzerland.
Address correspondence to:
Inke S. Näthke (inke{at}lifesci.dundee.ac.uk)
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