ArticleThe Journal of clinical investigation2015
Increased H3K9me3 drives dedifferentiated phenotype via KLF6 repression in liposarcoma.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Tumorigenesis of well-differentiated and dedifferentiated liposarcoma: 12q amplicon architecture, oncogenic cargo, and evolutionary progression.Cancer metastasis reviews · 2026Review
- Reprogramming in delipidated adipocytes: metabolism, regulation and progress.Cell death discovery · 2026Review
- Spatially-resolved single cell atlas of liposarcoma reveals lineage hierarchies, immune niches, and regulatory circuits.bioRxiv : the preprint server for biology · 2026Article
- Histone H3K9 Methylation Is Differentially Modified in Odontogenic Cyst and Tumors.European journal of dentistry · 2025Article
- A Nanostring gene expression approach identifies aggressive clinical behavior related genes in dedifferentiated liposarcoma.Scientific reports · 2025Article
- Deciphering the prognostic and therapeutic significance of BAG1 and BAG2 for predicting distinct survival outcome and effects on liposarcoma.Scientific reports · 2024Article
- Pim-1 kinase protects the liver from ischemia reperfusion injury by regulating dynamics-related protein 1.iScience · 2024Article
- Impact of supraphysiologic MDM2 expression on chromatin networks and therapeutic responses in sarcoma.Cell genomics · 2023Article
- Enhancer Coamplification and Hijacking Promote Oncogene Expression in Liposarcoma.Cancer research · 2023Article
- Distinct histone H3 modification profiles correlate with aggressive characteristics of salivary gland neoplasms.Scientific reports · 2022Article
- Experimental models of undifferentiated pleomorphic sarcoma and malignant peripheral nerve sheath tumor.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Targeting the MDM2-p53 pathway in dedifferentiated liposarcoma.Frontiers in oncology · 2022Review
- Epigenetics of Cutaneous Sarcoma.International journal of molecular sciences · 2021Review
- Recent Advancement in Atypical Lipomatous Tumor Research.International journal of molecular sciences · 2021Review
- H3K9me3, H3K36me3, and H4K20me3 Expression Correlates with Patient Outcome in Esophageal Squamous Cell Carcinoma as Epigenetic Markers.Digestive diseases and sciences · 2019Article
- Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma.Nature communications · 2019Article
- Methylation Patterns of Lys9 and Lys27 on Histone H3 Correlate with Patient Outcome in Gastric Cancer.Digestive diseases and sciences · 2019Article
- Krüppel-Like Factor 6 Is Required for Oxidative and Oncogene-Induced Cellular Senescence.Frontiers in cell and developmental biology · 2019Article
- Genomic profiling of dedifferentiated liposarcoma compared to matched well-differentiated liposarcoma reveals higher genomic complexity and a common origin.Cold Spring Harbor molecular case studies · 2018Article
- KLF6 depletion promotes NF-κB signaling in glioblastoma.Oncogene · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Liposarcoma (LPS) can be divided into 4 different subtypes, of which well-differentiated LPS (WDLPS) and dedifferentiated LPS (DDLPS) are the most common. WDLPS is typically low grade, whereas DDLPS is high grade, aggressive, and carries a worse prognosis. WDLPS and DDLPS frequently co-occur in patients. However, it is not clear whether DDLPS arises independently from WDLPS, or whether epigenomic alterations underly the histopathological differences of these subtypes. Here, we profiled 9 epigenetic marks in tumor samples from 151 patients with LPS and showed elevated trimethylation of histone H3 at Lys9 (H3K9me3) levels in DDLPS tumors. Integrated ChIP-seq and gene expression analyses of patient-derived cell lines revealed that H3K9me3 mediates differential regulation of genes involved in cellular differentiation and migration. Among these, Kruppel-like factor 6 (KLF6) was reduced in DDLPS, with increased H3K9me3 at associated regulatory regions. Pharmacologic inhibition of H3K9me3 with chaetocin decreased DDLPS proliferation and increased expression of the adipogenesis-associated factors PPARγ, CEBPα, and CEBPβ, suggesting that increased H3K9me3 may mediate DDLPS-associated aggressiveness and dedifferentiation properties. KLF6 overexpression partially phenocopied chaetocin treatment in DDLPS cells and induced phenotypic changes that were consistent with adipocytic differentiation, suggesting that the effects of increased H3K9me3 may be mediated through KLF6. In conclusion, we provide evidence of an epigenetic basis for the transition between WDLPS and DDLPS.
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Registered trials
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.