Evidence map›Paper›PMID 23645533›Full record

ArticleNeuro-oncology2013

CDH5 is specifically activated in glioblastoma stemlike cells and contributes to vasculogenic mimicry induced by hypoxia.

Xing-Gang Mao, Xiao-Yan Xue, Liang Wang, Xiang Zhang, Ming Yan, Yan-Yang Tu, Wei Lin, Xiao-Fan Jiang, Hong-Gang Ren, Wei Zhang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
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    Review
  14. Article
  15. Article
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44 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 1 country.

Xing-Gang MaoDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, No. 17 Changle West Road, Xi'an, Shaanxi Province 710032, China.
Xiao-Yan Xue
Liang Wang
Xiang Zhang
Ming Yan
Yan-Yang Tu
Wei Lin
Xiao-Fan Jiang
Hong-Gang Ren
Wei Zhang
Shao-Jun Song
Air Force Medical University · CNXijing Hospital · CNTang Du Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA proportion of glioblastoma stemlike cells (GSCs) expressing endothelial cell marker CDH5 (vascular-endothelial-cadherin or CD144) can transdifferentiate into endothelial cells and form blood vessels. However, the implications of CDH5 expression in gliomas and how it is regulated in GSCs remain to be clarified.

methodsThe mRNA and protein levels of CDH5 were detected in glioma samples and cultured cell lines, and the prognostic value of the CDH5 expression level for GBM patients was evaluated. Bioinformatics analysis was performed to reveal the potential functional roles of CDH5 in glioblastoma multiforme. Gene knockdown induced by short hairpin RNA, chromatin immunoprecipitation analysis, and a vasculogenic tube formation assay were performed to investigate the relationships among hypoxia, CDH5 expression level, and angiogenesis.

resultsCDH5 was overexpressed in gliomas, correlated with tumor grades, and was an independent adverse prognostic predictor for glioblastoma multiforme patients. CDH5 was specifically activated in GSCs but not in non-GSCs or neural stem cells, and CDH5(+) cells could produce xenografts in immunocompromised mice. Bioinformatics analysis demonstrated that CDH5 might interact directly with hypoxia-inducible factor (HIF)2α. CDH5 expression was significantly upregulated in GSCs, but not in non-GSCs or normal neural stem cells, under a 1% O2 condition. Both HIF1α and HIF2α positively regulated CDH5 level in GSCs and could bind to the promoter of CDH5. Furthermore, CDH5 contributed to the vasculogenic mimicry of GSCs, especially under hypoxic conditions.

conclusionsThe specific expression of CDH5 in GSCs may contribute to GSC-derived neovasculogenesis in glioblastoma multiforme, especially under hypoxic conditions, revealing novel tumorigenic mechanisms contributed by GSCs.

Indexed as

HypoxiaAdultAnimalsAntigens, CDApoptosisBlotting, WesternBrain NeoplasmsCadherin 5CadherinsCell ProliferationCells, CulturedChromatin ImmunoprecipitationEndothelium, VascularEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryAntigens, CDCadherin 5CadherinsHypoxia-Inducible Factor 1, alpha SubunitRNA, MessengerRNA, Small Interferingbioinformaticsbrain tumor stem cellscancer stem cellhypoxiaVE-cadherin

Identifiers

PMID23645533
PMCPMC3688011
OpenAlexW2105951972

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.