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Beatson Institute for Cancer Research, Garscube Estate, Bearsden, Glasgow G61 1BD, United Kingdom [G. W. M., K. B., A. W. W., M. C. F.]; Cancer Research Center, The Burnham Institute, La Jolla, California 92037 [T. P., E. R.]; Centre for Genome Research, University of Edinburgh, Kings Buildings, Edinburgh EH9 3JQ, United Kingdom [M. I. A.]
Although focal adhesion kinase (FAK) is elevated in epithelial cancers, it is not known whether FAK expression influences tumor development in vivo. We found that fak +/- heterozygous mice display reduced 7,12-dimethylbenz[a]anthracene-induced papilloma formation that correlates with reduced FAK protein expression in the skin. However, the frequency of malignant conversion of papillomas into carcinomas is indistinguishable in fak +/- mice and their wild-type fak +/+ littermates, most likely because papilloma FAK protein expression is elevated to wild-type levels. We also found that keratinocyte FAK protein expression is important for cellular responses downstream of ras in vitro (monitored by extracellular signal-regulated kinase activation after integrin engagement). Because 7,12-dimethylbenz[a]anthracene induces an activating mutation of H-ras, this provides one possible explanation for suppression of papilloma formation when FAK protein is limiting.
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