Evidence map›Paper›PMID 27965462›Full record

ArticleOncotarget2017

LEF1 reduces tumor progression and induces myodifferentiation in a subset of rhabdomyosarcoma.

Julia Dräger, Katja Simon-Keller, Tobias Pukrop, Florian Klemm, Jörg Wilting, Carsten Sticht, Kai Dittmann, Matthias Schulz, Ivo Leuschner, Alexander Marx and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Research Progress of LEF1 Gene in Malignant Tumors.Clinical Medicine Insights. Oncology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Tumor suppressive functions of WNT5A in rhabdomyosarcoma.International journal of oncology · 2022
    Article
  7. Review
  8. Spreading of IsolatedInternational journal of molecular sciences · 2020
    Article
  9. The anti-tumor growth effect of a novel agent DMAMCL in rhabdomyosarcoma in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2019
    Article
  10. Article
  11. 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 6 institutions in 1 country.

Julia DrägerDepartment of Human Genetics, University Medical Center, Göttingen 37073, Germany.
Katja Simon-KellerInstitute of Pathology, University Medical Center Mannheim, Mannheim 68167, Germany.
Tobias PukropClinic for Internal Medicine III, Hematology and Medical Oncology, University Regensburg, Regensburg 93053, Germany.
Florian KlemmDepartment of Hematology/Medical Oncology, University Medical Center Göttingen, Göttingen 37099, Germany.
Jörg WiltingInstitute of Anatomy and Cell Biology, University Medical Center Göttingen, Göttingen 37075, Germany.
Carsten StichtCenter of Medical Research, Bioinformatic and Statistic, Medical Faculty Mannheim, Mannheim 68167, Germany.
Kai DittmannInstitute for Cellular and Molecular Immunology, University Medical Center Göttingen, Göttingen 37073, Germany.
Matthias SchulzDepartment of Hematology/Medical Oncology, University Medical Center Göttingen, Göttingen 37099, Germany.
Ivo LeuschnerKiel Paediatric Tumor Registry, Department of Paediatric Pathology, University Hospital Schleswig-Holstein, Kiel 24105, Germany.
Alexander MarxInstitute of Pathology, University Medical Center Mannheim, Mannheim 68167, Germany.
Heidi HahnDepartment of Human Genetics, University Medical Center, Göttingen 37073, Germany.
Universitätsmedizin Göttingen · DEHeidelberg University · DEUniversity Hospital Heidelberg · DEUniversity Hospital Regensburg · DEUniversity Hospital Schleswig-Holstein · DEUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and show characteristics of skeletal muscle differentiation. The two major RMS subtypes in children are alveolar (ARMS) and embryonal RMS (ERMS). We demonstrate that approximately 50% of ARMS and ERMS overexpress the LEF1/TCF transcription factor LEF1 when compared to normal skeletal muscle and that LEF1 can restrain aggressiveness especially of ARMS cells. LEF1 knockdown experiments in cell lines reveal that depending on the cellular context, LEF1 can induce pro-apoptotic signals. LEF1 can also suppress proliferation, migration and invasiveness of RMS cells both in vitro and in vivo. Furthermore, LEF1 can induce myodifferentiation of the tumor cells. This may involve regulation of other LEF1/TCF factors i.e. TCF1, whereas β-catenin activity plays a subordinate role. Together these data suggest that LEF1 rather has tumor suppressive functions and attenuates aggressiveness in a subset of RMS.

Indexed as

ApoptosisBiomarkers, TumorBiopsyCell DifferentiationCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene ExpressionGene Knockdown TechniquesHumansLymphoid Enhancer-Binding Factor 1Neoplasm GradingRhabdomyosarcomaTissue Array AnalysisWnt Signaling PathwayBiomarkers, TumorLEF1 protein, humanLymphoid Enhancer-Binding Factor 1LEF1/TCFRMSWNT/β-catenin signaling

Identifiers

PMID27965462
PMCPMC5356880
OpenAlexW2560238097

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.