ArticlePloS one2008
FUS-DDIT3 prevents the development of adipocytic precursors in liposarcoma by repressing PPARgamma and C/EBPalpha and activating eIF4E.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Challenges and hope: latest research trends in the clinical treatment and prognosis of liposarcoma.Frontiers in pharmacology · 2025Review
- Mechanism of efficacy of trabectedin against myxoid liposarcoma entails detachment of the FUS-DDIT3 transcription factor from its DNA binding sites.Journal of experimental & clinical cancer research : CR · 2024Article
- FUS::DDIT3 Fusion Protein in the Development of Myxoid Liposarcoma and Possible Implications for Therapy.Biomolecules · 2024Review
- Primary Orbital Myxoid Liposarcoma.Medical sciences (Basel, Switzerland) · 2023Article
- Suppression of antitumor cytokine IL‑24 by PRG4 and PAI‑1 may promote myxoid liposarcoma cell survival.Biomedical reports · 2023Article
- Small Non-Coding RNAs in Soft-Tissue Sarcomas: State of the Art and Future Directions.Molecular cancer research : MCR · 2023Review
- The Recent Advances in Molecular Diagnosis of Soft Tissue Tumors.International journal of molecular sciences · 2023Review
- Fusion protein-driven IGF-IR/PI3K/AKT signals deregulate Hippo pathway promoting oncogenic cooperation of YAP1 and FUS-DDIT3 in myxoid liposarcoma.Oncogenesis · 2022Article
- Establishment and evaluation of retroperitoneal liposarcoma patient-derived xenograft models: an ideal model for preclinical study.International journal of medical sciences · 2022Article
- Rationale for Early Detection ofCancers · 2021Review
- Suppression of MKL1 promotes adipocytic differentiation and reduces the proliferation of myxoid liposarcoma cells.Oncology letters · 2020Article
- FusionPathway: Prediction of pathways and therapeutic targets associated with gene fusions in cancer.PLoS computational biology · 2018Article
- High-Throughput Screening of Myxoid Liposarcoma Cell Lines: Survivin Is Essential for Tumor Growth.Translational oncology · 2017Article
- Establishment and characterization of a new human myxoid liposarcoma cell line (DL-221) with the FUS-DDIT3 translocation.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Article
- Extensive lipoma-like changes of myxoid liposarcoma: morphologic, immunohistochemical, and molecular cytogenetic analyses.Virchows Archiv : an international journal of pathology · 2015Article
- Advances in the targeted therapy of liposarcoma.OncoTargets and therapy · 2015Review
- Mode of action of trabectedin in myxoid liposarcomas.Oncogene · 2014Article
- The role of mesenchymal stem/progenitor cells in sarcoma: update and dispute.Stem cell investigation · 2014Review
- Mesenchymal stem cell transformation and sarcoma genesis.Clinical sarcoma research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFUS-DDIT3 is a chimeric protein generated by the most common chromosomal translocation t(12;16)(q13;p11) linked to liposarcomas, which are characterized by the accumulation of early adipocytic precursors. Current studies indicate that FUS-DDIT3- liposarcoma develops from uncommitted progenitors. However, the precise mechanism whereby FUS-DDIT3 contributes to the differentiation arrest remains to be elucidated. METHODOLOGY/PRINCIPAL
findingsHere we have characterized the adipocyte regulatory protein network in liposarcomas of FUS-DITT3 transgenic mice and showed that PPARgamma2 and C/EBPalpha expression was altered. Consistent with in vivo data, FUS-DDIT3 MEFs and human liposarcoma cell lines showed a similar downregulation of both PPARgamma2 and C/EBPalpha expression. Complementation studies with PPARgamma but not C/EBPalpha rescued the differentiation block in committed adipocytic precursors expressing FUS-DDIT3. Our results further show that FUS-DDIT3 interferes with the control of initiation of translation by upregulation of the eukaryotic translation initiation factors eIF2 and eIF4E both in FUS-DDIT3 mice and human liposarcomas cell lines, explaining the shift towards the truncated p30 isoform of C/EBPalpha in liposarcomas. Suppression of the FUS-DDIT3 transgene did rescue this adipocyte differentiation block. Moreover, eIF4E was also strongly upregulated in normal adipose tissue of FUS-DDIT3 transgenic mice, suggesting that overexpression of eIF4E may be a primary event in the initiation of liposarcomas. Reporter assays showed FUS-DDIT3 is involved in the upregulation of eIF4E in liposarcomas and that both domains of the fusion protein are required for affecting eIF4E expression. CONCLUSIONS/SIGNIFICANCE: Taken together, this study provides evidence of the molecular mechanisms involve in the disruption of normal adipocyte differentiation program in liposarcoma harbouring the chimeric gene FUS-DDIT3.
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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.