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The Bmi-1/NF-kappa B/VEGF story: another hint for proteasome involvement in glioma angiogenesis?
dc.creator | Vlachostergios, P. J. | en |
dc.creator | Papandreou, C. N. | en |
dc.date.accessioned | 2015-11-23T10:53:47Z | |
dc.date.available | 2015-11-23T10:53:47Z | |
dc.date.issued | 2013 | |
dc.identifier | 10.1007/s12079-013-0198-2 | |
dc.identifier.issn | 1873-9601 | |
dc.identifier.uri | http://hdl.handle.net/11615/34528 | |
dc.description.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-kappa B/VEGF pathway in promoting glioma cell-mediated tubule formation and migration of endothelial cells and neovascularization both in vitro and in vivo. NF-kappa B inhibition reversed these effects, supporting a role for Bmi-1 in glioma angiogenesis. Given the intimate association of Bmi-1 and NF-kappa B 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. | en |
dc.source.uri | <Go to ISI>://WOS:000209420900002 | |
dc.subject | Bmi-1 | en |
dc.subject | NF-kappa B | en |
dc.subject | VEGF | en |
dc.subject | Glioma | en |
dc.subject | Ubiquitin-proteasome system | en |
dc.subject | Proteasome | en |
dc.subject | inhibitor | en |
dc.subject | Cell Biology | en |
dc.title | The Bmi-1/NF-kappa B/VEGF story: another hint for proteasome involvement in glioma angiogenesis? | en |
dc.type | journalArticle | en |
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