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Specific deletion of focal adhesion kinase suppresses tumor formation and blocks malignant progression

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    Rights statement: Copyright © 2004, Cold Spring Harbor Laboratory Press

    Final published version, 317 KB, PDF document

Original languageEnglish
Pages (from-to)2998-3003
Number of pages6
JournalGenes & Development
Issue number24
Publication statusPublished - 15 Dec 2004


We have generated mice with a floxed fak allele under the control of keratin-14-driven Cre fused to a modified estrogen receptor (CreER(T2)). 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.

    Research areas

  • 9,10-Dimethyl-1,2-benzanthracene, Animals, Apoptosis, Blotting, Western, DNA Primers, Flow Cytometry, Fluorescent Antibody Technique, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Gene Deletion, Genotype, Hydroxytestosterones, Immunohistochemistry, Integrases, Keratin-14, Keratinocytes, Keratins, Mice, Mice, Transgenic, Neoplasm Metastasis, Protein-Tyrosine Kinases, Receptors, Estrogen, Skin Neoplasms, Tamoxifen

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