Evidence map›Paper›PMID 18223685›Full record

ArticleOncogene2008

Endoglin expression in metastatic breast cancer cells enhances their invasive phenotype.

D Oxmann, J Held-Feindt, A M Stark, K Hattermann, T Yoneda, R Mentlein

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Mutant p53 promotes tumor progression and metastasis by the endoplasmic reticulum UDPase ENTPD5.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Metastasis review: from bench to bedside.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  18. Article
  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

6 authors at 4 institutions in 2 countries.

D OxmannDepartment of Anatomy, University of Kiel, Kiel, Germany.
J Held-Feindt
A M Stark
K Hattermann
T Yoneda
R Mentlein
Kiel University · DEThe University of Texas Health Science Center at San Antonio · USUniversity Hospital Schleswig-Holstein · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoglin is a cell-surface adhesion protein as well as a coreceptor for transforming growth factor-beta (TGF-beta). It is located on endothelial and few other cells, but also found on certain tumor cells. Brain metastatic breast tumor cells derived from the MDA-MB-231 cell line heavily express endoglin in contrast to the corresponding parental ones. To clarify whether this determines their invasive phenotype, we compared their biological properties with endoglin-silenced brain-metastatic cells, low-expressing parental cells and these transfected with L- and S-endoglins, isoforms transducing or lacking TGF-beta signals. All L-endoglin-overexpressing cells were characterized by numerous invadopodia where endoglin was preferentially localized. Endoglin-expression resulted in elevated levels of the matrix metalloproteinases (MMP-1 and MMP-19) and downregulation of the plasminogen activator inhibitor-1. In Boyden-chamber and wound-healing assays, endoglin-overexpressing cells showed a considerably higher migration and chemotaxis to TGF-beta. In 3D spheroid confrontation assays between breast tumor cells and TGF-beta-secreting glioma cells, high L-endoglin-expressing cells invaded into the glioma-spheroids whereas low-endoglin-expressing cells dissociated in the culture; invasion was blocked by TGF-beta antibodies. In contrast to parental cells, endoglin-overexpressing cells invaded deeply into mouse brain slices. Thus, endoglin expression on tumor cells enhances their invasive character by formation of invadopodia, extracellular proteolysis, chemotaxis and migration.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntigens, CDCell Line, TumorCell MovementEndoglinGliomaHumansIntracellular Signaling Peptides and ProteinsMatrix Metalloproteinase 1Matrix Metalloproteinases, SecretedMiceNeoplasm InvasivenessNeoplasm MetastasisPhenotypeReceptors, Cell SurfaceAntigens, CDEndoglinENG protein, humanEng protein, mouseIntracellular Signaling Peptides and ProteinsMatrix Metalloproteinase 1matrix metalloproteinase 19Matrix Metalloproteinases, SecretedReceptors, Cell SurfaceTransforming Growth Factor beta

Identifiers

PMID18223685
OpenAlexW2052507160

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.