Open AccessThe Bmi‐1/NF‐κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis?
Author(s) -
Vlachostergios Panagiotis J.,
Papandreou Christos N.
Publication year - 2013
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-013-0198-2
Subject(s) - angiogenesis , glioma , cancer research , neovascularization , carcinogenesis , cell growth , biology , cancer , medicine , genetics
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.