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Tumor Biology |
Laboratory of Molecular Neuro-Oncology, Department of Neurosurgery and Hematology/Oncology (F.W.K., E.A.S., S.L.M), and Pathology (D.J.B.), Winship Cancer Institute (B.K., E.G.V.M.), Emory University School of Medicine, Atlanta, GA 30322, USA
2 Address correspondence to Erwin G. Van Meir, Winship Cancer Institute, Emory University School of Medicine, 1365C Clifton Road, NE, Room C5078, Atlanta, GA 30322, USA (evanmei{at}emory.edu).
Abstract
Glioblastomas, like other solid tumors, have extensive areas of hypoxia and
necrosis. The importance of hypoxia in driving tumor growth is receiving
increased attention. Hypoxia-inducible factor 1 (HIF-1) is one of the master
regulators that orchestrate the cellular responses to hypoxia. It is a
heterodimeric transcription factor composed of 
and ß subunits.
The subunit is stable in hypoxic conditions but is rapidly degraded in
normoxia. The function of HIF-1 is also modulated by several molecular
mechanisms that regulate its synthesis, degradation, and transcriptional
activity. Upon stabilization or activation, HIF-1 translocates to the nucleus
and induces transcription of its downstream target genes. Most important to
gliomagenesis, HIF-1 is a potent activator of angiogenesis and invasion
through its upregulation of target genes critical for these functions.
Activation of the HIF-1 pathway is a common feature of gliomas and may explain
the intense vascular hyperplasia often seen in glioblastoma multiforme.
Activation of HIF results in the activation of vascular endothelial growth
factors, vascular endothelial growth factor receptors, matrix
metalloproteinases, plasminogen activator inhibitor, transforming growth
factors and ß, angiopoietin and Tie receptors, endothelin-1,
inducible nitric oxide synthase, adrenomedullin, and erythropoietin, which all
affect glioma angiogenesis. In conclusion, HIF is a critical regulatory factor
in the tumor microenvironment because of its central role in promoting
proangiogenic and invasive properties. While HIF activation strongly promotes
angiogenesis, the emerging vasculature is often abnormal, leading to a vicious
cycle that causes further hypoxia and HIF upregulation.
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