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.
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Vlachostergios, P.J., Papandreou, C.N. The Bmi-1/NF-κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis?. J. Cell Commun. Signal. 7, 235–237 (2013). https://doi.org/10.1007/s12079-013-0198-2
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DOI: https://doi.org/10.1007/s12079-013-0198-2
Keywords
- Bmi-1
- NF-κB
- VEGF
- Glioma
- Ubiquitin-proteasome system
- Proteasome inhibitor