ArticleClinical orthopaedics and related research2014
Loss of SS18-SSX1 inhibits viability and induces apoptosis in synovial sarcoma.
Article in Clinical orthopaedics and related research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 36 citations in OpenAlex.
- MicroRNA-29b-5p regulates cell proliferation and cancer stemness via TGF-β/p300 pathway in human synovial sarcoma.Cancer cell international · 2026Article
- Targeting SUMOylation promotes cBAF complex stabilization and disruption of the SS18::SSX transcriptome in synovial sarcoma.Nature communications · 2025Article
- Functional Classification of Fusion Proteins in Sarcoma.Cancers · 2024Review
- Review
- Expression of gasdermin D in clear cell renal cell carcinoma and its effect on its biological function.Frontiers in oncology · 2023Article
- Genotyping of Circulating Free DNA Enables Monitoring of Tumor Dynamics in Synovial Sarcomas.Cancers · 2022Article
- SYT-SSX1 enhances the invasiveness and maintains stem-like cell properties in synovial sarcoma via induction of TGF-β1/Smad signaling.BMC cancer · 2022Article
- Molecular mechanisms underpinning sarcomas and implications for current and future therapy.Signal transduction and targeted therapy · 2021Review
- HDAC2 links ubiquitination to tumor suppression in synovial sarcoma.Molecular & cellular oncology · 2021Article
- The Long-Term Outcomes of Intensive Combined Therapy of Adult Patients with Localised Synovial Sarcoma.Journal of clinical medicine · 2020Article
- Article
- Targeting the undruggable: exploiting neomorphic features of fusion oncoproteins in childhood sarcomas for innovative therapies.Cancer metastasis reviews · 2019Review
- HDAC2 Regulates Site-Specific Acetylation of MDM2 and Its Ubiquitination Signaling in Tumor Suppression.iScience · 2019Article
- Article
- Proteomic signatures corresponding to the SS18/SSX fusion gene in synovial sarcoma.Oncotarget · 2018Article
- Article
- Soft Tissue Sarcoma Cancer Stem Cells: An Overview.Frontiers in oncology · 2018Review
- Identification of SHCBP1 as a novel downstream target gene of SS18-SSX1 and its functional analysis in progression of synovial sarcoma.Oncotarget · 2016Article
- Preclinical Evidence of Anti-Tumor Activity Induced by EZH2 Inhibition in Human Models of Synovial Sarcoma.PloS one · 2016Article
- Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundMost synovial sarcomas contain a chromosomal translocation t(X;18), which results in the formation of an oncoprotein SS18-SSX critical to the viability of synovial sarcoma. QUESTIONS/PURPOSES: We (1) established and characterized three novel synovial sarcoma cell lines and asked (2) whether inhibition of SS18-SSX1 decreases cell viability in these cell lines; and (3) whether reduction in viability after SS18-SSX1 knockdown is caused by apoptosis. After identifying a specific posttranscriptional splice variant in our cell lines, we asked (4) whether this provides a survival benefit in synovial sarcoma.
methodsCells lines were characterized. SS18-SSX1 knockdown was achieved using a shRNA system. Cell viability was assessed by WST-1 analysis and apoptosis examined by caspase-3 activity.
resultsWe confirmed the SS18-SSX1 translocation in all cell lines and identified a consistent splicing variant. We achieved successful knockdown of SS18-SSX1 and with this saw a significant reduction in cell viability. Decreased viability was a result of increased apoptosis. Reintroduction of the exon 8 sequence into cells reduced cell viability in all cell lines.
conclusionsWe confirmed the presence of the SS18-SSX1 translocation in our cell lines and its importance in the survival of synovial sarcoma. We have also demonstrated that reduction in cell viability is related to an increase in apoptosis. In addition, we have identified a potential mediator of SS18-SSX function in exon 8. CLINICAL RELEVANCE: SS18-SSX represents a tumor-specific target in synovial sarcoma. Exploitation of SS18-SSX and its protein partners will allow us to develop potent tumor-specific therapeutic agents.
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