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RESEARCH COMMUNICATION
1 The Beatson Institute for Cancer Research, Garscube Estate, Bearsden, Glasgow, G61 1BD, United Kingdom; 2 Institute of Biological and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom; 3 Wellcome Trust Sanger Institute, Cambridgeshire, CB10 1XA, United Kingdom; 4 Division of Neuroscience, University of Edinburgh, Edinburgh, EH8 9JZ, United Kingdom; 5 The London Queen Mary's School of Medicine and Dentistry, John Vane Science Centre, London, EC1M 6BQ, United Kingdom; 6 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, Collège de France, 67404 Illkirch Cedex, Strasbourg, France
We have generated mice with a floxed fak allele under the control of keratin-14-driven Cre fused to a modified estrogen receptor (CreERT2). 4-Hydroxy-tamoxifen treatment induced fak deletion in the epidermis, and suppressed chemically induced skin tumor formation. Loss of fak induced once benign tumors had formed inhibited malignant progression. Although fak deletion was associated with reduced migration of keratinocytes in vitro, we found no effect on wound re-epithelialization in vivo. However, increased keratinocyte cell death was observed after fak deletion in vitro and in vivo. Our work provides the first experimental proof implicating FAK in tumorigenesis, and this is associated with enhanced apoptosis.
[Keywords: Focal adhesion kinase; conditional; cancer; keratinocyte; apoptosis]
Received July 1, 2004; revised version accepted October 14, 2004.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.316304.
8 Corresponding author.
E-MAIL g.mclean{at}beatson.gla.ac.uk; FAX 44-141-942-6521.
7 Present address: Chiba-City Kaihin Hospital, 3-31-1 Isobe, Mihama-Ku, Chiba City, Japan.
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