Evidence map›Paper›PMID 23375101›Full record

ReviewThe FEBS journal2013

Synstatin: a selective inhibitor of the syndecan-1-coupled IGF1R-αvβ3 integrin complex in tumorigenesis and angiogenesis.

Alan C Rapraeger

Abstract readReview
In one paragraph

Review in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. SSTNSignal transduction and targeted therapy · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Syndecan-1 (CD138), Carcinomas and EMT.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Alan C RapraegerDepartment of Human Oncology, Carbone Comprehensive Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin-Madison, Madison, WI 53705, USA. rapraeger@humonc.wisc.edu
University of Wisconsin Carbone Cancer Center · US

Funding

Synstatin Therapy for Multiple MyelomaR01CA139872 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2010 to 2014
$1.9M
Proteoglycans of the Plasma MembraneR01CA109010 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2004 to 2008
$1.2M
Regulation of angiogenesis by syndecan-1R01CA118839 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2006 to 2009
$1.0M
NCI NIH HHS R01 CA109010NCI NIH HHS R01-CA109010NCI NIH HHS R01 CA118839NCI NIH HHS R01-CA119939NCI NIH HHS R01 CA139872NCI NIH HHS R01-CA139872
6 · The paper itself

Abstract

The syndecans are a family of heparan sulfate-decorated cell-surface proteoglycans: matrix receptors with roles in cell adhesion and growth factor signaling. Their heparan sulfate chains recognize 'heparin-binding' motifs that are ubiquitously present in the extracellular matrix, providing the means for syndecans to constitutively bind and cluster to sites of cell-matrix adhesion. Emerging evidence suggests that specialized docking sites in the syndecan extracellular domains may serve to localize other receptors to these sites as well, including integrins and growth factor receptor tyrosine kinases. A prototype of this mechanism is capture of the αvβ3 integrin and insulin-like growth factor 1 receptor (IGF1R) by syndecan-1 (Sdc1), forming a ternary receptor complex in which signaling downstream of IGF1R activates the integrin. This Sdc1-coupled ternary receptor complex is especially prevalent on tumor cells and activated endothelial cells undergoing angiogenesis, reflecting the up-regulated expression of αvβ3 integrin in such cells. As such, much effort has focused on developing therapeutic agents that target this integrin in various cancers. Along these lines, the site in the Sdc1 ectodomain that is responsible for capture and activation of the αvβ3 or αvβ5 integrins by IGF1R can be mimicked by a short peptide called 'synstatin', which competitively displaces the integrin and IGF1R kinase from the syndecan and inactivates the complex. This review summarizes our current knowledge of the Sdc1-coupled ternary receptor complex and the efficacy of synstatin as an emerging therapeutic agent to target this signaling mechanism.

Indexed as

Cell Transformation, NeoplasticAnimalsAntigens, CDCadherin 5CadherinsCell AdhesionEndothelial CellsHumansIntegrin alphaVbeta3MiceNeovascularization, PathologicPeptidesProtein BindingReceptor, IGF Type 1Recombinant ProteinsSyndecan-1Antigens, CDCadherin 5CadherinsIntegrin alphaVbeta3PeptidesReceptor, IGF Type 1Recombinant ProteinsSDC1 protein, humanSyndecan-1Ternary Complex Factors

Identifiers

PMID23375101
PMCPMC3651771
OpenAlexW2087356589

What OpenQuestion holds

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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.