Evidence map›Paper›PMID 20383200›Full record

ArticleOncogene2010

Nodal promotes growth and invasion in human gliomas.

C-C Lee, H-J Jan, J-H Lai, H-I Ma, D-Y Hueng, Y-C Gladys Lee, Y-Y Cheng, L-W Liu, H-W Wei, H-M Lee

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. The TGF-β Family in Glioblastoma.International journal of molecular sciences · 2024
    Review
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  5. Role ofMolecular biology research communications · 2021
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  10. Article
  11. Article
  12. Review
  13. Article
  14. Exogenous Cripto-1 Suppresses Self-Renewal of Cancer Stem Cell Model.International journal of molecular sciences · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Nodal signalling and asymmetry of the nervous system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  19. Article
  20. 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

10 authors at 6 institutions in 1 country.

C-C LeeDepartment of Pathology, Shin Kong Memorial Hospital, Taipei, Taiwan.
H-J Jan
J-H Lai
H-I Ma
D-Y Hueng
Y-C Gladys Lee
Y-Y Cheng
L-W Liu
H-W Wei
H-M Lee
Taipei Medical University · TWCentral Taiwan University of Science and Technology · TWNational Defense Medical Center · TWNational Taiwan University of Science and Technology · TWShin Kong WHS Memorial Hospital · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrolled growth and diffused invasion are major causes of mortality in patients with malignant gliomas. Nodal has been shown to have a central role in the tumorigenic signaling pathways of malignant melanoma. In this study, we show that grade IV human glioma cell lines expressed different levels of Nodal, paralleled to the potential for cell invasiveness. Treatment of glioma cell lines with recombinant Nodal (rNodal) increased matrix metalloproteinase 2 (MMP-2) secretion and cell invasiveness. The ectopic expression of Nodal in GBM glioma cells that expressed Nodal at low level resulted in increased MMP-2 secretion, enhanced cell invasiveness, raised cell proliferation rates in vitro, increased tumor growth in vivo, and was associated with poor survival in a mice xenograft model. In contrast, the knockdown of Nodal expression in U87MG glioma cells with high Nodal expression level had reduced MMP-2 secretion, less cell invasiveness, lower tumor growth in vivo and longer lifespan in mice with U87MG/shNodal cell xenografts. In addition, Nodal knockdown promoted the reversion of malignant glioma cells toward a differentiated astrocytic phenotype. Furthermore, our data support the notion that Nodal may regulate glioma progression through the induction of the leukemia inhibitory factor (LIF) and Cripto-1 through activated Smad.

Indexed as

AnimalsCell DivisionCell Line, TumorCentral Nervous System NeoplasmsDisease ProgressionEpidermal Growth FactorGene Expression Regulation, NeoplasticGene Knockout TechniquesGliomaGPI-Linked ProteinsHumansIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsLeukemia Inhibitory FactorMatrix Metalloproteinase 2Membrane GlycoproteinsEpidermal Growth FactorGPI-Linked ProteinsIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsLeukemia Inhibitory FactorLIF protein, humanMatrix Metalloproteinase 2Membrane GlycoproteinsMembrane ProteinsNeoplasm ProteinsNOMO3 protein, humanRecombinant ProteinsSmad ProteinsTDGF1 protein, humanTissue Inhibitor of Metalloproteinase-2

Identifiers

PMID20383200
OpenAlexW1986792117

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.