ArticleNature communications2025
Aberrant EZHIP expression drives tumorigenesis in osteosarcoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed.
- CXorf67 in malignancies: Deciphering epigenetic landscapes and clinical implications for precision oncology.Genes & diseases · 2026Review
- Single-cell fixed RNA profiling of the osteosarcoma clinical Spectrum identifies ADAMTS12 and RNASE1 as key drivers of the metastatic niche.Journal of bone oncology · 2026Article
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- SETD2 methyltransferase activity promotes correct transcription initiation and termination.EMBO reports · 2026Article
- Integrating single-cell and bulk transcriptomes to reveal prognostic and immunological features of ecDNA-related genes in osteosarcoma.Cancer immunology, immunotherapy : CII · 2026Article
- Article
- EZHIP in Pediatric Brain Tumors: From Epigenetic Mimicry to Therapeutic Vulnerabilities.International journal of molecular sciences · 2026Review
- Dynamic evolution of EZHIP, an inhibitor of the Polycomb Repressive Complex 2 in mammals.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors.
Funding
Abstract
Osteosarcomas (OS) are aggressive bone tumors known for their extensive structural variations and rare recurrent oncogenic driver mutations. In this study, we identify ectopic expression of the oncohistone-mimic EZHIP in 20% of patients across two independent OS cohorts. We demonstrate that reduced deposition of the repressive H3K27me3 mark correlates with poor histological response to neoadjuvant therapy, serving as a predictor of patient outcomes. Through gain- and loss-of-function experiments, we provide functional evidence of the oncogenic activity of EZHIP in enhancing the aggressive characteristics of OS both in vitro and in vivo. EZHIP-induced epigenetic reprogramming reactivates developmental pathways and impedes the differentiation of mesenchymal progenitors, pushing them towards smooth muscle lineage commitment at the cost of other fates. Targeting residual H3K27me3 with EZH2 inhibitors may offer therapeutic benefit in EZHIP-expressing OS. Our findings highlight EZHIP expression as a prevalent driver in OS, offering insights into its pathogenic mechanisms and potential therapeutic strategies for this debilitating cancer.
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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.