Evidence map›Paper›PMID 17496924›Full record

ArticleOncogene2007

Endoglin inhibits prostate cancer motility via activation of the ALK2-Smad1 pathway.

C S Craft, D Romero, C P H Vary, R C Bergan

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. ALK1Fc Suppresses the Human Prostate Cancer Growth inFrontiers in cell and developmental biology · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Prostate cancer: the need for biomarkers and new therapeutic targets.Journal of Zhejiang University. Science. B · 2014
    Review
  17. Improved survival outcomes in cancer patients with hereditary hemorrhagic telangiectasia.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    Article
  18. An orthotopic murine model of human prostate cancer metastasis.Journal of visualized experiments : JoVE · 2013
    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

4 authors at 2 institutions in 1 country.

C S CraftDivision of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Northwestern University and the Robert H Lurie Cancer Center of Northwestern University, Chicago, IL, USA.
D Romero
C P H Vary
R C Bergan
Maine Medical Center Research Institute · USNorthwestern University · US

Funding

SUPPRESSIVE ROLE OF ANDROGEN RESPONSE GENE CALRETICULIN IN PROSTATE CANCERP50CA090386 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CRAWFORD, SUSAN · 2001 to 2013
$25.1M
Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
Regulation of TGF-beta Receptor-dependent Vascular DiseaseR01HL083151 · NHLBI · MAINEHEALTH · PI VARY, CALVIN PARDEE HULL · 2007 to 2011
$2.0M
NCI NIH HHS CA90386NCI NIH HHS P50 CA090386NCI NIH HHS T32 CA009560NCI NIH HHS T32CA09560NCRR NIH HHS P20 RR015555NHLBI NIH HHS R01 HL083151
6 · The paper itself

Abstract

Endoglin is a transforming growth factor beta (TGFbeta) superfamily auxiliary receptor. We had previously shown that it suppressed prostate cancer (PCa) cell motility, and that its expression was lost during PCa progression. The mechanism by which endoglin inhibits PCa cell motility is unknown. Here we demonstrate that endoglin abrogates TGFbeta-mediated cell motility, but does not alter cell surface binding of TGFbeta. By measuring Smad-specific phosphorylation and Smad-responsive promoter activity, endoglin was shown to constitutively activate Smad1, with little-to-no effect upon Smad3. Knockdown of Smad1 increased motility and abrogated endoglin's effects. As type I activin receptor-like kinases (ALKs) are necessary for Smad activation, we went on to show that knockdown of ALK2, but not TGFbetaRI (ALK5), abrogated endoglin-mediated decreases in cell motility and constitutively active ALK2 was sufficient to restore a low-motility phenotype in endoglin deficient cells. These findings provide the first evidence that endoglin decreases PCa cell motility through activation of the ALK2-Smad1 pathway.

Indexed as

Activin Receptors, Type IAntigens, CDBlotting, WesternCell Line, TumorCell MovementEndoglinFlow CytometryHumansMaleProstatic NeoplasmsReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionSmad1 ProteinActivin Receptors, Type IACVR1 protein, humanAntigens, CDEndoglinENG protein, humanReceptors, Cell SurfaceSmad1 ProteinSMAD1 protein, human

Identifiers

PMID17496924
PMCPMC2199239
OpenAlexW2092873962

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.