Evidence map›Paper›PMID 20153339›Full record

ArticleMicrovascular research2010

Role of endothelial cell-selective adhesion molecule in hematogeneous metastasis.

Husni M Cangara, Tatsuro Ishida, Tetsuya Hara, Li Sun, Ryuji Toh, Yoshiyuki Rikitake, Ramendra K Kundu, Thomas Quertermous, Ken-ichi Hirata, Yoshitake Hayashi

Open access · greenAbstract read
In one paragraph

Article in Microvascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Resolving neutrophils due to TRAM deletion renders protection against experimental sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Role of the blood-brain barrier in the formation of brain metastases.International journal of molecular sciences · 2013
    Review
  12. Article
  13. Article
  14. 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 2 institutions in 3 countries.

Husni M CangaraDivision of Molecular Medicine and Genetics, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Tatsuro Ishida
Tetsuya Hara
Li Sun
Ryuji Toh
Yoshiyuki Rikitake
Ramendra K Kundu
Thomas Quertermous
Ken-ichi Hirata
Yoshitake Hayashi
Kobe University · JPStanford University · US

Funding

Endothelial Basis of the Apelin-APJ PathwayR01HL077676 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2005 to 2008
$1.5M
NHLBI NIH HHS R01 HL077676
6 · The paper itself

Abstract

The spread of malignant cells from a localized tumor is thought to be directly related to the number of microvessels in the tumor. The endothelial cell-selective adhesion molecule (ESAM) is a member of the immunoglobulin superfamily that mediates homophilic interactions between endothelial cells. Previous studies have indicated that ESAM regulates angiogenesis in the primary tumor growth and endothelial permeability. In this study, we aimed to further elucidate the role of ESAM in tumor metastasis through angiogenic processes. ESAM expression was higher in hypervascular metastatic tumor tissues than in normal tissues in human lungs. Cell culture studies found that conditioned medium from B16F10 melanoma cells increased ESAM expression in endothelial cells and promoted endothelial migration and tube formation. The B16F10 medium-induced endothelial migration and tube formation were significantly attenuated when ESAM was downregulated by siRNA transfection. Intravenous injection of B16F10 cells into ESAM+/+ and ESAM-/- mice for comparison of metastatic potential resulted in the number of metastatic lung nodules in ESAM-/- mice being 83% lower than of those in ESAM+/+ mice. The microvascular density in the tumor was also lower in ESAM-/- than in ESAM+/+ mice. These findings indicate that ESAM regulates tumor metastasis through endothelial cell migration and tube formation in metastatic nodules. Inhibition of ESAM may therefore inhibit tumor metastasis by inhibiting the angiogenic processes.

Indexed as

AnimalsApoptosisCell Adhesion MoleculesCell LineCell Line, TumorCell MovementCulture Media, ConditionedEndothelial CellsHumansLung NeoplasmsMelanoma, ExperimentalMiceMice, Inbred StrainsMice, KnockoutNeoplasm ProteinsNeovascularization, PathologicCell Adhesion MoleculesCulture Media, ConditionedEsam protein, mouseESM1 protein, humanNeoplasm ProteinsProteoglycansRNA, Small Interfering

Identifiers

PMID20153339
PMCPMC5316236
OpenAlexW2065165331

What OpenQuestion holds

Textmetadata
LicenceTDM
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.