Evidence map›Paper›PMID 23212305›Full record

ArticleClinical & experimental metastasis2013

L1CAM stimulates glioma cell motility and proliferation through the fibroblast growth factor receptor.

Vishnu Mohanan, Murali K Temburni, John C Kappes, Deni S Galileo

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. L1CAM promotes ovarian cancer stemness and tumor initiation via FGFR1/SRC/STAT3 signaling.Journal of experimental & clinical cancer research : CR · 2021
    Article
  14. Review
  15. Review
  16. Role of Exosomes in the Progression, Diagnosis, and Treatment of Gliomas.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  17. Review
  18. Article
  19. Characterization of molecular signatures of supratentorial ependymomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    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 3 institutions in 1 country.

Vishnu MohananDepartment of Biological Sciences, University of Delaware, Newark, DE 19716, USA.
Murali K Temburni
John C Kappes
Deni S Galileo
University of Delaware · USDelaware State University · USUniversity of Alabama at Birmingham · US

Funding

VOLUMETRIC BREAST DENSITY ESTIMATION USING BREAST SURFACE RECONSTRUCTEDP20RR016472 · NCRR · UNIVERSITY OF DELAWARE · PI STANHOPE, STEVEN J. · 2001 to 2011
$37.6M
Mucosal HIV and Immunobiology CenterR24DK064400 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SMITH, PHILLIP D · 2003 to 2012
$4.8M
NCRR NIH HHS 2 P20 RR016472NIDDK NIH HHS R24 DK64400
6 · The paper itself

Abstract

The L1CAM cell adhesion/recognition molecule (L1, CD171) and fibroblast growth factor receptor (FGFR) both are expressed by human high-grade glioma cells, but their potential actions in controlling cell behavior have not been linked. L1 actions in cancer cells have been attributed mainly to integrin receptors, and we demonstrated previously that L1-stimulated glioma cell migration correlates with integrin expression, increased focal adhesion kinase activation and focal complex turnover. Our analyses of datasets revealed FGFR is overexpressed in glioma regardless of grade, while ADAM10 metalloprotease expression increases with glioma grade. Here, we used dominant-negative and short hairpin RNA approaches to inhibit the activation of FGFR1 and expression of L1, respectively. An L1 peptide that inhibits L1-FGFR interaction and PD173074, a chemical inhibitor of FGFR1 activity, also were used to elucidate the involvement of L1-FGFR interactions on glioma cell behavior. Time-lapse cell motility studies and flow cytometry cell cycle analyses showed that L1 operates to increase glioma cell motility and proliferation through FGFR activation. Shutdown of both L1 expression and FGFR activity in glioma cells resulted in a complete termination of cell migration in vitro. These studies show for the first time that soluble L1 ectodomain (L1LE) acts on glioma cells through FGFRs, and that FGFRs are used by glioma cells for increasing motility as well as proliferation in response to activation by L1LE ligand. Thus, effective treatment of high-grade glioma may require simultaneous targeting of L1, FGFRs, and integrin receptors, which would reduce glioma cell motility as well as proliferation.

Indexed as

Cell MovementCell ProliferationADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesApoptosisBlotting, WesternBrain NeoplasmsCell CycleFlow CytometryGliomaHumansMembrane ProteinsNeoplasm GradingNeural Cell Adhesion Molecule L1Peptide FragmentsADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesFGFR1 protein, humanMembrane ProteinsNeural Cell Adhesion Molecule L1PD 173074Peptide FragmentsPyrimidinesReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID23212305
OpenAlexW2019009843

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.