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The proto-oncogene c-myc is involved in the regulation of cell proliferation, differentiation, and apoptosis. In this study, we used an inducible transgenic mouse model in which c-Myc was targeted to the epidermis and, after activation, gave rise to hyperplastic and dysplastic skin lesions and to dermal angiogenesis, involving both vascular endothelial growth factor (VEGF) receptor-1 and VEGF receptor-2. After c-Myc activation, VEGF mRNA was expressed in postmitotic keratinocytes where it colocalized with transgene expression and areas of tissue hypoxia, suggesting a role of hypoxia in VEGF induction. In vitro, c-Myc activation alone was able to induce VEGF protein release and in conjunction with hypoxia, c-Myc activation further increased VEGF protein. Blocking VEGF signaling in vivo significantly reduced dermal angiogenesis, demonstrating the importance of VEGF as a mediating factor for the c-Myc-induced angiogenic phenotype.

Original publication




Journal article


Cancer Res

Publication Date





6563 - 6570


Animals, Cell Hypoxia, Hypoxia-Inducible Factor 1, alpha Subunit, Indoles, Keratinocytes, Mice, Neovascularization, Physiologic, Papilloma, Precancerous Conditions, Proto-Oncogene Proteins c-myc, Pyrroles, RNA, Messenger, Skin, Skin Neoplasms, Tamoxifen, Transcription Factors, Transgenes, Vascular Endothelial Growth Factor A