Evidence map›Paper›PMID 25749382›Full record

ArticleOncotarget2015

The histone code reader SPIN1 controls RET signaling in liposarcoma.

Henriette Franz, Holger Greschik, Dominica Willmann, Luka Ozretić, Cordula Annette Jilg, Eva Wardelmann, Manfred Jung, Reinhard Buettner, Roland Schüle

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  4. Immune-modulatory effects of Spindlin-1 inhibitors.Clinical and experimental immunology · 2025
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  7. An integrated structural model of the DNA damage-responsive H3K4me3 binding WDR76:SPIN1 complex with the nucleosome.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  9. Review
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  15. Driving integrative structural modeling with serial capture affinity purification.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

9 authors at 5 institutions in 1 country.

Henriette FranzUrologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany.
Holger GreschikUrologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany.
Dominica WillmannUrologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany.
Luka OzretićUniversitätsklinikum Köln, Institut für Pathologie, Köln, Germany.
Cordula Annette JilgUrologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany.
Eva WardelmannUniversitätsklinikum Münster, Gerhard-Domagk-Insitut für Pathologie, Münster, Germany.
Manfred JungInstitut für Pharmazeutische Wissenschaften, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
Reinhard BuettnerUniversitätsklinikum Köln, Institut für Pathologie, Köln, Germany.
Roland SchüleUrologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany.
University Medical Center Freiburg · DECentrum für Integrierte Onkologie · DEGerman Marine Research Consortium · DEUniversity Hospital Münster · DEUniversity of Freiburg · DE

Funding

European Research Council 322844
6 · The paper itself

Abstract

The histone code reader Spindlin1 (SPIN1) has been implicated in tumorigenesis and tumor growth, but the underlying molecular mechanisms remain poorly understood. Here, we show that reducing SPIN1 levels strongly impairs proliferation and increases apoptosis of liposarcoma cells in vitro and in xenograft mouse models. Combining signaling pathway, genome-wide chromatin binding, and transcriptome analyses, we found that SPIN1 directly enhances expression of GDNF, an activator of the RET signaling pathway, in cooperation with the transcription factor MAZ. Accordingly, knockdown of SPIN1 or MAZ results in reduced levels of GDNF and activated RET explaining diminished liposarcoma cell proliferation and survival. In line with these observations, levels of SPIN1, GDNF, activated RET, and MAZ are increased in human liposarcoma compared to normal adipose tissue or lipoma. Importantly, a mutation of SPIN1 within the reader domain interfering with chromatin binding reduces liposarcoma cell proliferation and survival. Together, our data describe a molecular mechanism for SPIN1 function in liposarcoma and suggest that targeting SPIN1 chromatin association with small molecule inhibitors may represent a novel therapeutic strategy.

Indexed as

Signal TransductionAdipose TissueAnimalsApoptosisBlotting, WesternCell Cycle ProteinsCell ProliferationChromatin ImmunoprecipitationFluorescent Antibody TechniqueHistone CodeHumansImmunoenzyme TechniquesImmunoprecipitationLipomaLiposarcomaMiceCell Cycle ProteinsMicrotubule-Associated ProteinsPhosphoproteinsProto-Oncogene Proteins c-retRET protein, humanRNA, MessengerRNA, Small InterferingspindlinGDNFhistone code readerMAZRET signalingSPIN1

Identifiers

PMID25749382
PMCPMC4467114
OpenAlexW1559920963

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.