Bmi-1 Promotes Glioma Angiogenesis by Activating NF-κB Signaling

Lili Jiang, Libing Song, Jueheng Wu, Yi Yang, Xun Zhu, Bo Hu, Shi Yuan Cheng, Mengfeng Li*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Angiogenesis in glioma is associated with the poor prognosis of the disease and closely correlates with the highly invasive phenotype of glioma cells, which represents the most challenging impediment against the currently glioma treatments. Bmi-1, an onco-protein, has been implicated in the progression of various human cancers, including gliomas, whereas its role in glioma angiogenesis remains unclear. Our current study examined the effects of Bmi-1 on glioma angiogenesis in vitro as well as in vivo. We found that overexpression of Bmi-1 enhanced, whereas knockdown of Bmi-1 diminished, the capability of glioma cells to induce tubule formation and migration of endothelial cells and neovascularization in chicken chorioallantoic membrane. In vivo, Bmi-1 overexpression and knockdown, respectively, promoted and inhibited angiogenesis in orthotopically transplanted human gliomas. Furthermore, NF-κB activity and VEGF-C expression was induced by Bmi-1 overexpression, whereas Bmi-1 knockdown attenuated NF-κB signaling and decreased VEGF-C expression. Additionally suppression of NF-κB activity using a specific chemical inhibitor abrogated the NF-κB activation and the pro-angiogenic activities of glioma cells. Together, our data suggest that Bmi-1 plays an important role in glioma angiogenesis and therefore could represent a potential target for anti-angiogenic therapy against the disease.

Original languageEnglish (US)
Article numbere55527
JournalPloS one
Issue number1
StatePublished - Jan 31 2013

ASJC Scopus subject areas

  • General


Dive into the research topics of 'Bmi-1 Promotes Glioma Angiogenesis by Activating NF-κB Signaling'. Together they form a unique fingerprint.

Cite this