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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Breast Neoplasms, Cell Line, Tumor, Cell Movement, Down-Regulation, Enzyme Activation, Fibroblast Growth Factor 7, Focal Adhesion Protein-Tyrosine Kinases, GRB2 Adaptor Protein, Humans, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Nuclear Proteins, Phosphorylation, Recombinant Proteins, Signal Transduction.
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Do wilms ' tumor 1 protein and focal adhesion kinase mediate keratinocyte growth factor signaling in breast cancer cells? Context: Keratinocyte growth factor (KGF) has been shown to induce breast cancer metastasis in animal models. cDNA microarrays have revealed that KGF increased Wilms tumor 1 (WT1) and focal adhesion kinase (FAK) expression in breast cancer cells. The role of WT1 and FAK in KGF signaling was investigated. A cell culture wounding model was used to study the effects of WT1 and FAK down-regulation on KGF-induced proliferation and motility in breast cancer cells. WT1 down-regulation inhibited KGF-mediated proliferation and motility of breast cancer cells, while FAK down-regulation inhibited proliferation, but had no significant effect on cell motility. WT1 down-regulation, but not FAK down-regulation, led to Erk1,2 inactivation.
assistant
KGF-mediated signaling employs WT1 and FAK to regulate breast cancer cell proliferation and motility and may represent therapeutic targets for the prevention of breast cancer progression. Final Decision: yes