Evidence map›Paper›PMID 21116837›Full record

ArticleJournal of neuro-oncology2011

Inhibition of Nodal suppresses angiogenesis and growth of human gliomas.

Dueng-Yuan Hueng, Gu-Jiun Lin, Shing-Hwa Huang, Li-Wen Liu, Da-Tong Ju, Yuan-Wu Chen, Huey-Kang Sytwu, Chen Chang, Shih-Ming Huang, Yi-Shian Yeh and 2 more

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. ID1Cell death & disease · 2024
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  17. DDX3X Biomarker Correlates with Poor Survival in Human Gliomas.International journal of molecular sciences · 2015
    Article
  18. Article
  19. Article
  20. Expression and significance of Nodal in human cancers: a meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
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

12 authors at 6 institutions in 1 country.

Dueng-Yuan HuengDepartment of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, 325, Sec. 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Gu-Jiun Lin
Shing-Hwa Huang
Li-Wen Liu
Da-Tong Ju
Yuan-Wu Chen
Huey-Kang Sytwu
Chen Chang
Shih-Ming Huang
Yi-Shian Yeh
Horng-Mo Lee
Hsin-I Ma
National Defense Medical Center · TWTri-Service General Hospital · TWCentral Taiwan University of Science and Technology · TWInstitute of Biomedical Sciences, Academia Sinica · TWTaipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is the hallmark of malignant gliomas positively correlated with the vascular endothelial growth factor (VEGF) expression. We previously reported that expression levels of Nodal, a member of transforming growth factor-β super family, correlate with the malignant invasive behavior of human glioma cells. In this study, we show that knockdown of Nodal suppresses glioma angiogenesis by inhibition of VEGF. In human primary glioma specimens, expression of Nodal positively correlates with WHO glioma tumor grades and expression of VEGF in the corresponding glioma specimens. In human U87MG glioma cells, knockdown of endogenous Nodal by RNA interference (RNAi) significantly decreases colony formation and secretion of VEGF. In vivo, cellular depletion of Nodal in U87MG inhibited brain glioma growth and prolonged the survival of mice with U87MG/shNodal glioma compared with controls. Inhibition of Nodal suppressed tumor vessel growth in U87MG gliomas. Using Nodal inhibitor (SB431542), silencing Nodal, or overexpressing Nodal in the U87MG, GBM8401, and GBM glioma cells, our further experiments revealed that Nodal-induced VEGF expression might, at least in part, mediate through the ERK1/2-HIF-1α-mediated signaling pathway. Taken together, our data revealed that alteration of Nodal expression in glioma cells resulted in changes to VEGF secretion, and subsequent colony formation, in vivo tumor growth, and angiogenesis, all of which are consistent with the regulation of VEGF through the ERK1/2-HIF-1α-mediated signaling, suggesting that Nodal may serve as a potential therapeutic target for the treatment of human gliomas.

Indexed as

Analysis of VarianceAnimalsBenzamidesBrain NeoplasmsCell Line, TransformedCell ProliferationComputational BiologyDioxolesDose-Response Relationship, DrugEnzyme InhibitorsEnzyme-Linked Immunosorbent AssayFlavonoidsGene Expression Regulation, NeoplasticGliomaHumansHypoxia-Inducible Factor 1, alpha Subunit2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideBenzamidesDioxolesEnzyme InhibitorsFlavonoidsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNodal ProteinNODAL protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor A

Identifiers

PMID21116837
OpenAlexW2169465089

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.