Evidence map›Paper›PMID 23383216›Full record

ArticlePloS one2013

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

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 51 citations in OpenAlex.

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  19. Bmi-1 serves as a potential novel marker for progression in human cutaneous basal cell carcinoma.International journal of clinical and experimental pathology · 2017
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Lili JiangDepartment of Pathophysiology, Guangzhou Medical University, Guangzhou, Guangdong, China.
Libing Song
Jueheng Wu
Yi Yang
Xun Zhu
Bo Hu
Shi-Yuan Cheng
Mengfeng Li
Sun Yat-sen University · CNNorthwestern University · USGuangzhou Medical University · CN

Funding

Modulation of Oncogenic Signaling in GlioblastomasR01CA159811 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN · 2012 to 2016
$1.8M
ELMO1, Dock180 and Glioma InvasionR01CA130966 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHENG, SHI-YUAN · 2008 to 2012
$1.5M
NCI NIH HHS R01 CA130966NCI NIH HHS R01 CA159811
6 · The paper itself

Abstract

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.

Indexed as

Signal TransductionAnimalsCell Line, TumorChick EmbryoEnzyme ActivationGene ExpressionGene SilencingGliomaHumansMiceNeovascularization, PathologicNF-kappa BPolycomb Repressive Complex 1RNA InterferenceTransplantation, HeterologousVascular Endothelial Growth Factor CBMI1 protein, humanNF-kappa BPolycomb Repressive Complex 1Vascular Endothelial Growth Factor C

Identifiers

PMID23383216
PMCPMC3561301
OpenAlexW2166222647

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.