ArticleJournal of cell communication and signaling2013
The Bmi-1/NF-κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis?
Article in Journal of cell communication and signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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.
Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Genetic Variants of BMI1 (rs1042059 and rs11591377) and Their Potential Role in Leukemia Susceptibility: A Narrative Review.Health science reports · 2026Article
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- Overexpression of α-Synuclein Reorganises Growth Factor Profile of Human Astrocytes.Molecular neurobiology · 2021Article
- Article
- BMI-1, a promising therapeutic target for human cancer.Oncology letters · 2015Article
- Evaluating the Oxidative Stress in Inflammation: Role of Melatonin.International journal of molecular sciences · 2015Review
- Expression of β-transducin repeat-containing E3 ubiquitin protein ligase in human glioma and its correlation with prognosis.Oncology letters · 2015Article
- URG4/URGCP enhances the angiogenic capacity of human hepatocellular carcinoma cells in vitro via activation of the NF-κB signaling pathway.BMC cancer · 2015Article
- Article
- Ubiquitin-specific protease 22: a novel molecular biomarker in glioma prognosis and therapeutics.Medical oncology (Northwood, London, England) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Identifiers
What OpenQuestion holds
Registered trials
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.