Fiche publication
Date publication
décembre 2004
Journal
Genes & development
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre
,
Dr METZGER Daniel
Tous les auteurs :
McLean GW, Komiyama NH, Serrels B, Asano H, Reynolds L, Conti F, Hodivala-Dilke K, Metzger D, Chambon P, Grant SG, Frame MC
Lien Pubmed
Résumé
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.
Mots clés
9,10-Dimethyl-1,2-benzanthracene, toxicity, Animals, Apoptosis, genetics, Blotting, Western, DNA Primers, Flow Cytometry, Fluorescent Antibody Technique, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Gene Deletion, Genotype, Hydroxytestosterones, metabolism, Immunohistochemistry, Integrases, metabolism, Keratin-14, Keratinocytes, physiology, Keratins, metabolism, Mice, Mice, Transgenic, Neoplasm Metastasis, genetics, Protein-Tyrosine Kinases, genetics, Receptors, Estrogen, metabolism, Skin Neoplasms, chemically induced, Tamoxifen, analogs & derivatives
Référence
Genes Dev.. 2004 Dec;18(24):2998-3003
