The Bmi-1/NF-κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis? Academic Article uri icon

Overview

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.

publication date

  • March 15, 2013

Identity

PubMed Central ID

  • PMC3889254

Scopus Document Identifier

  • 84891372302

Digital Object Identifier (DOI)

  • 10.1002/1097-0142(20000601)88:11<2606::AID-CNCR25>3.0.CO;2-W

PubMed ID

  • 23494769

Additional Document Info

volume

  • 7

issue

  • 4