Evidence map›Paper›PMID 20856203›Full record

ArticleOncogene2011

Critical role of endoglin in tumor cell plasticity of Ewing sarcoma and melanoma.

E Pardali, D W J van der Schaft, E Wiercinska, A Gorter, P C W Hogendoorn, A W Griffioen, P ten Dijke

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.2field-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

45 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Endoglin and squamous cell carcinomas.Frontiers in medicine · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review
  14. Review
  15. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  16. Role of immunotherapy in Ewing sarcoma.Journal for immunotherapy of cancer · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

E PardaliDepartment of Molecular Cell Biology, Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands. E.Pardali@lumc.nl
D W J van der Schaft
E Wiercinska
A Gorter
P C W Hogendoorn
A W Griffioen
P ten Dijke
Leiden University Medical Center · NLAmsterdam UMC Location VUmc · NLEindhoven University of Technology · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cell plasticity enables certain types of highly malignant tumor cells to dedifferentiate and engage a plastic multipotent embryonic-like phenotype, which enables them to 'adapt' during tumor progression and escape conventional therapeutic strategies. This plastic phenotype of aggressive cancer cells enables them to express endothelial cell-specific markers and form tube-like structures, a phenotype that has been linked to aggressive behavior and poor prognosis. We demonstrate here that the transforming growth factor (TGF)-β co-receptor endoglin, an endothelial cell marker, is expressed by tumor cells and its expression correlates with tumor cell plasticity in two types of human cancer, Ewing sarcoma and melanoma. Moreover, endoglin expression was significantly associated with worse survival of Ewing sarcoma patients. Endoglin knockdown in tumor cells interferes with tumor cell plasticity and reduces invasiveness and anchorage-independent growth in vitro. Ewing sarcoma and melanoma cells with reduced endoglin levels showed reduced tumor growth in vivo. Mechanistically, we provide evidence that endoglin, while interfering with TGF-β signaling, is required for efficient bone morphogenetic protein, integrin, focal adhesion kinase and phosphoinositide-3-kinase signaling in order to maintain tumor cell plasticity. The present study delineates an important role of endoglin in tumor cell plasticity and progression of aggressive tumors.

Indexed as

AnimalsAntigens, CDBase SequenceBone Morphogenetic ProteinsCell DivisionCell Line, TumorDNA PrimersEndoglinFemaleFocal Adhesion Protein-Tyrosine KinasesGene Knockdown TechniquesHumansImmunohistochemistryMelanomaMiceMice, NudeAntigens, CDBone Morphogenetic ProteinsDNA PrimersEndoglinENG protein, humanFocal Adhesion Protein-Tyrosine KinasesPhosphatidylinositol 3-KinasesReceptors, Cell SurfaceTransforming Growth Factor beta

Identifiers

PMID20856203
OpenAlexW2141474130

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.