| First Author | Tang N | Year | 2004 |
| Journal | Cancer Cell | Volume | 6 |
| Issue | 5 | Pages | 485-95 |
| PubMed ID | 15542432 | Mgi Jnum | J:94773 |
| Mgi Id | MGI:3521513 | Doi | 10.1016/j.ccr.2004.09.026 |
| Citation | Tang N, et al. (2004) Loss of HIF-1alpha in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis. Cancer Cell 6(5):485-95 |
| abstractText | We deleted the hypoxia-responsive transcription factor HIF-1alpha in endothelial cells (EC) to determine its role during neovascularization. We found that loss of HIF-1alpha inhibits a number of important parameters of EC behavior during angiogenesis: these include proliferation, chemotaxis, extracellular matrix penetration, and wound healing. Most strikingly, loss of HIF-1alpha in EC results in a profound inhibition of blood vessel growth in solid tumors. These phenomena are all linked to a decreased level of VEGF expression and loss of autocrine response of VEGFR-2 in HIF-1alpha null EC. We thus show that a HIF-1alpha-driven, VEGF-mediated autocrine loop in EC is an essential component of solid tumor angiogenesis. |
