title: The Bmi-1/NF-κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis?
abstract: Angiogenesis is an essential process for sustaining tumor growth, particularly in cancer cell types with rapid proliferation, including malignant glioma. Bmi-1 is a transcriptional regulator of the polycomb group involved in repression of gene expression by altering the state of chromatin at specific promoters. Bmi-1 overexpression was previously implicated in glioma tumorigenesis, proliferation, self-renewal, apoptotic resistance and invasiveness. In a recent study, Jiang et al. (PLoS One 8:e55527, 2013) have revealed the involvement of Bmi-1/NF-κB/VEGF pathway in promoting glioma cell-mediated tubule formation and migration of endothelial cells and neovascularization both in vitro and in vivo. NF-κB inhibition reversed these effects, supporting a role for Bmi-1 in glioma angiogenesis. Given the intimate association of Bmi-1 and NF-κB with the ubiquitin-proteasome system, a better understanding of protein turnover in angiogenic signaling, discussed here, provides novel implications for anti-angiogenic treatment strategies in gliomas.
authors.affiliation: Department of Medical Oncology, Faculty of Medicine, University of Thessaly, University Hospital of Larissa, Biopolis, 41110, Larissa, Greece, pvlacho@med.uth.gr.
authors.forename: Panagiotis J
authors.initials: PJ
authors.lastname: Vlachostergios
authors.forename: Christos N
authors.initials: CN
authors.lastname: Papandreou