Evidence map›Paper›PMID 38041233›Full record

ArticleCancer science2024

TGF-β signaling promotes desmoid tumor formation via CSRP2 upregulation.

Yu Li, Teruaki Fujishita, Emi Mishiro-Sato, Yasushi Kojima, Yanqing Niu, Makoto Mark Taketo, Yuya Urano, Tomohisa Sakai, Atsushi Enomoto, Yoshihiro Nishida and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. CSRP2 modulates PDGFRA/PI3K/AKT signaling via PRC1 components in glioma.Cellular oncology (Dordrecht, Netherlands) · 2026
    Article
  3. Article
  4. 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

11 authors at 4 institutions in 1 country.

Yu LiDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Teruaki FujishitaDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID https://orcid.org/0000-0002-4397-2438
Emi Mishiro-SatoDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Yasushi KojimaDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID https://orcid.org/0000-0002-0087-1768
Yanqing NiuDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Makoto Mark TaketoColon Cancer Project, Kyoto University Hospital-iACT, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yuya UranoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tomohisa SakaiDepartment of Orthopedic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-9206-6116
Yoshihiro NishidaDepartment of Rehabilitation, Nagoya University Hospital, Nagoya, Japan.ORCID https://orcid.org/0000-0002-7511-6388
Masahiro AokiDivision of Pathophysiology, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID https://orcid.org/0000-0003-4316-9490
Aichi Cancer Center · JPNagoya University · JPKyoto University Hospital · JPNagoya University Hospital · JP

Funding

Japan Society for the Promotion of Science JP17H01585Japan Society for the Promotion of Science JP18H02686Japan Society for the Promotion of Science JP20K07440
6 · The paper itself

Abstract

Desmoid tumors (DTs), also called desmoid-type fibromatoses, are locally aggressive tumors of mesenchymal origin. In the present study, we developed a novel mouse model of DTs by inducing a local mutation in the Ctnnb1 gene, encoding β-catenin in PDGFRA-positive stromal cells, by subcutaneous injection of 4-hydroxy-tamoxifen. Tumors in this model resembled histologically clinical samples from DT patients and showed strong phosphorylation of nuclear SMAD2. Knockout of SMAD4 in the model significantly suppressed tumor growth. Proteomic analysis revealed that SMAD4 knockout reduced the level of Cysteine-and-Glycine-Rich Protein 2 (CSRP2) in DTs, and treatment of DT-derived cells with a TGF-β receptor inhibitor reduced CSRP2 RNA levels. Knockdown of CSRP2 in DT cells significantly suppressed their proliferation. These results indicate that the TGF-β/CSRP2 axis is a potential therapeutic target for DTs downstream of TGF-β signaling.

Indexed as

Desmoid TumorsAnimalsbeta CateninHumansLIM Domain ProteinsMiceMice, KnockoutMuscle ProteinsNuclear ProteinsProteomicsTransforming Growth Factor betaUp-Regulationbeta CateninCSRP2 protein, humanCsrp2 protein, mouseLIM Domain ProteinsMuscle ProteinsNuclear ProteinsTransforming Growth Factor betadesmoid tumorsfibrosismouse modelsTGF-βWnt signaling

Identifiers

PMID38041233
PMCPMC10859603
OpenAlexW4389267848

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.