Evidence map›Paper›PMID 25405986›Full record

ArticlePloS one2014

Myofibroblast-derived SFRP1 as potential inhibitor of colorectal carcinoma field effect.

Gábor Valcz, Arpád V Patai, Alexandra Kalmár, Bálint Péterfia, István Fűri, Barnabás Wichmann, Györgyi Műzes, Ferenc Sipos, Tibor Krenács, Emese Mihály and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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  11. Transcriptomic Profiling for the Autophagy Pathway in Colorectal Cancer.International journal of molecular sciences · 2020
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  15. Up-regulation ofJournal of Cancer · 2019
    Article
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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

13 authors at 3 institutions in 2 countries.

Gábor ValczMolecular Medicine Research Unit, Hungarian Academy of Sciences, Budapest, Hungary.
Arpád V Patai2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Alexandra Kalmár2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Bálint Péterfia2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
István Fűri2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Barnabás WichmannMolecular Medicine Research Unit, Hungarian Academy of Sciences, Budapest, Hungary.
Györgyi Műzes2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Ferenc Sipos2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Tibor Krenács1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Emese Mihály2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Sándor SpisákDana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, United States of America.
Béla MolnárMolecular Medicine Research Unit, Hungarian Academy of Sciences, Budapest, Hungary; 2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Zsolt TulassayMolecular Medicine Research Unit, Hungarian Academy of Sciences, Budapest, Hungary; 2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUHungarian Academy of Sciences · HUHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic changes of stromal-epithelial interactions are of key importance in the regulation of colorectal carcinoma (CRC) cells and morphologically normal, but genetically and epigenetically altered epithelium in normal adjacent tumor (NAT) areas. Here we demonstrated retained protein expression of well-known Wnt inhibitor, secreted frizzled-related protein 1 (SFRP1) in stromal myofibroblasts and decreasing epithelial expression from NAT tissues towards the tumor. SFRP1 was unmethylated in laser microdissected myofibroblasts and partially hypermethylated in epithelial cells in these areas. In contrast, we found epigenetically silenced myofibroblast-derived SFRP1 in CRC stroma. Our results suggest that the myofibroblast-derived SFRP1 protein might be a paracrine inhibitor of epithelial proliferation in NAT areas and loss of this signal may support tumor proliferation in CRC.

Indexed as

CarcinomaColorectal NeoplasmsDNA MethylationGene Expression Regulation, NeoplasticGene SilencingHCT116 CellsHumansIntercellular Signaling Peptides and ProteinsMembrane ProteinsMyofibroblastsSecreted Frizzled-Related ProteinsIntercellular Signaling Peptides and ProteinsMembrane ProteinsSecreted Frizzled-Related ProteinsSFRP1 protein, human

Identifiers

PMID25405986
PMCPMC4236006
OpenAlexW2112968112

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.