| First Author | Knies-Bamforth UE | Year | 2004 |
| Journal | Cancer Res | Volume | 64 |
| Issue | 18 | Pages | 6563-70 |
| PubMed ID | 15374969 | Mgi Jnum | J:93664 |
| Mgi Id | MGI:3487344 | Doi | 10.1158/0008-5472.CAN-03-3176 |
| Citation | Knies-Bamforth UE, et al. (2004) c-Myc interacts with hypoxia to induce angiogenesis in vivo by a vascular endothelial growth factor-dependent mechanism. Cancer Res 64(18):6563-70 |
| abstractText | 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. |
