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[Cancer Research 61, 8385-8389, December 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Decreased Focal Adhesion Kinase Suppresses Papilloma Formation during Experimental Mouse Skin Carcinogenesis1

Gordon W. McLean2, Ken Brown3, Margaret I. Arbuckle, Anne W. Wyke, Timo Pikkarainen4, Erkki Ruoslahti and Margaret C. Frame

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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