Evidence map›Paper›PMID 23448253›Full record

ArticleThe FEBS journal2013

Decorin interferes with platelet-derived growth factor receptor signaling in experimental hepatocarcinogenesis.

Kornélia Baghy, Zsolt Horváth, Eszter Regős, Katalin Kiss, Zsuzsa Schaff, Renato V Iozzo, Ilona Kovalszky

Abstract read
In one paragraph

Article 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 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Decorin: matrix-based pan-cancer tumor suppressor.Molecular and cellular biochemistry · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Decorin deficiency promotes epithelial-mesenchymal transition and colon cancer metastasis.Matrix biology : journal of the International Society for Matrix Biology · 2021
    Article
  15. Article
  16. The liver fibrosis niche: Novel insights into the interplay between fibrosis-composing mesenchymal cells, immune cells, endothelial cells, and extracellular matrix.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    Review
  17. Article
  18. Review
  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

7 authors at 2 institutions in 2 countries.

Kornélia Baghy1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Zsolt Horváth
Eszter Regős
Katalin Kiss
Zsuzsa Schaff
Renato V Iozzo
Ilona Kovalszky
Semmelweis University · HUSidney Kimmel Cancer Center · US

Funding

NEOPLASTIC MODULATION OF PROTEOGLYCAN METABOLISMR01CA039481 · NCI · UNIVERSITY OF PENNSYLVANIA · PI IOZZO, RENATO V. · 1985 to 2020
$7.1M
NCI NIH HHS R01 CA039481NCI NIH HHS R01 CA39481
6 · The paper itself

Abstract

Decorin, a secreted small leucine-rich proteoglycan, acts as a tumor repressor in a variety of cancers, mainly by blocking the action of several receptor tyrosine kinases such as the receptors for hepatocyte, epidermal and insulin-like growth factors. In the present study we investigated the effects of decorin in an experimental model of thioacetamide-induced hepatocarcinogenesis and its potential role in modulating the signaling of platelet-derived growth factor receptor-α (PDGFRα). Genetic ablation of decorin in mice led to enhanced tumor prevalence and a higher tumor count compared with wild-type mice. These findings correlated with decreased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) and concurrent activation (phosphorylation) of PDGFRα in the hepatocellular carcinomas generated in the decorin-null vis-à-vis wild-type mice. Notably, in normal liver PDGFRα localized primarily to the membrane of nonparenchymal cells, whereas in the malignant counterpart PDGFRα was expressed by the malignant cells at their cell surfaces. This process was facilitated by a genetic background lacking endogenous decorin. Double immunostaining of the proteoglycan and the receptor revealed only minor colocalization, leading to the hypothesis that decorin would bind to the natural ligand PDGF rather than to the receptor itself. Indeed, we found, using purified proteins and immune-blot assays, that decorin binds to PDGF. Collectively, our findings support the idea that decorin acts as a secreted tumor repressor during hepatocarcinogenesis by hindering the action of another receptor tyrosine kinase, such as the PDGFRα, and could be a novel therapeutic agent in the battle against liver cancer.

Indexed as

Signal TransductionAnimalsCyclin-Dependent Kinase Inhibitor p21DecorinFemaleFluorescent Antibody TechniqueHepatocytesHumansLigandsLiverLiver Neoplasms, ExperimentalMaleMiceMice, Inbred C57BLPhosphorylationPlatelet-Derived Growth FactorCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Dcn protein, mouseDecorinLigandsPlatelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor alphaRecombinant ProteinsThioacetamideTumor Suppressor Proteins

Identifiers

PMID23448253
PMCPMC3651810
OpenAlexW2086189483

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.