Evidence map›Paper›PMID 24166495›Full record

ArticleOncogene2014

SS18-SSX fusion protein-induced Wnt/β-catenin signaling is a therapeutic target in synovial sarcoma.

M Trautmann, E Sievers, S Aretz, D Kindler, S Michels, N Friedrichs, M Renner, J Kirfel, S Steiner, S Huss and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.7field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Combination of HDAC and FYN inhibitors in synovial sarcoma treatment.Frontiers in cell and developmental biology · 2024
    Article
  10. Review
  11. Review
  12. Article
  13. SS18-SSX drives CREB activation in synovial sarcoma.Cellular oncology (Dordrecht, Netherlands) · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
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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

22 authors at 8 institutions in 3 countries.

M Trautmann1] Department of Pathology, University Hospital Cologne, Cologne, Germany [2] Department of Pathology, University Hospital Bonn, Bonn, Germany.
E SieversDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
S AretzInstitute of Human Genetics, University of Bonn, Bonn, Germany.
D KindlerDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
S MichelsDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
N FriedrichsDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
M RennerDepartment of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
J KirfelDepartment of Pathology, University Hospital Bonn, Bonn, Germany.
S SteinerDepartment of Pathology, University Hospital Bonn, Bonn, Germany.
S HussDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
A KochDepartment of Neuropathology, Charité-Universitätsmedizin, Berlin, Germany.
R PenzelDepartment of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
O LarssonDepartments of Oncology & Pathology, The Karolinska Institute, Stockholm, Sweden.
A KawaiDivision of Orthopaedic Surgery, National Cancer Center Hospital, Tokyo, Japan.
S TanakaLaboratory of Molecular & Cellular Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
H SonobeDepartment of Laboratory Medicine, Chungoku Central Hospital, Fukuyama, Hiroshima, Japan.
A WahaDepartment of Neuropathology, University Hospital Bonn, Bonn, Germany.
P SchirmacherDepartment of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
G MechtersheimerDepartment of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
E WardelmannDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
R BüttnerDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
W HartmannDepartment of Pathology, University Hospital Cologne, Cologne, Germany.
University Hospital Cologne · DEHeidelberg University · DEUniversity Hospital Bonn · DECharité - Universitätsmedizin Berlin · DEHokkaido University · JPKarolinska Institutet · SEUniversity Hospital Heidelberg · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial sarcoma is a high-grade soft tissue malignancy characterized by a specific reciprocal translocation t(X;18), which leads to the fusion of the SS18 (SYT) gene to one of three SSX genes (SSX1, SSX2 or SSX4). The resulting chimeric SS18-SSX protein is suggested to act as an oncogenic transcriptional regulator. Despite multimodal therapeutic approaches, metastatic disease is often lethal and the development of novel targeted therapeutic strategies is required. Several expression-profiling studies identified distinct gene expression signatures, implying a consistent role of Wnt/β-catenin signaling in synovial sarcoma tumorigenesis. Here we investigate the functional and therapeutic relevance of Wnt/β-catenin pathway activation in vitro and in vivo. Immunohistochemical analyses of nuclear β-catenin and Wnt downstream targets revealed activation of canonical Wnt signaling in a significant subset of 30 primary synovial sarcoma specimens. Functional aspects of Wnt signaling including dependence of Tcf/β-catenin complex activity on the SS18-SSX fusion proteins were analyzed. Efficient SS18-SSX-dependent activation of the Tcf/β-catenin transcriptional complex was confirmed by TOPflash reporter luciferase assays and immunoblotting. In five human synovial sarcoma cell lines, inhibition of the Tcf/β-catenin protein-protein interaction significantly blocked the canonical Wnt/β-catenin signaling cascade, accompanied by the effective downregulation of Wnt targets (AXIN2, CDC25A, c-MYC, DKK1, CyclinD1 and Survivin) and the specific suppression of cell viability associated with the induction of apoptosis. In SYO-1 synovial sarcoma xenografts, administration of small molecule Tcf/β-catenin complex inhibitors significantly reduced tumor growth, associated with diminished AXIN2 protein levels. In summary, SS18-SSX-induced Wnt/β-catenin signaling appears to be of crucial biological importance in synovial sarcoma tumorigenesis and progression, representing a potential molecular target for the development of novel therapeutic strategies.

Indexed as

Wnt Signaling PathwayAnimalsAntineoplastic Agentsbeta CateninCell Line, TumorCell NucleusCell SurvivalGene ExpressionHEK293 CellsHumansMaleMice, Inbred BALB CMice, NudeOncogene Proteins, FusionPerylenePyrimidinonesAntineoplastic Agentsbeta CateninCGP049090CTNNB1 protein, humanOncogene Proteins, FusionPerylenePKF115-584PKF118-310PyrimidinonesSS18-SSX1 fusion proteinSYT-SSX fusion proteinTriazines

Identifiers

PMID24166495
OpenAlexW1976626755

What OpenQuestion holds

Textmetadata
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.