ArticleCell death & disease2021
The incorporation loci of H3.3K36M determine its preferential prevalence in chondroblastomas.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Histone tail mutants: versatile tools for decoding chromatin, development, and disease.Trends in genetics : TIG · 2026Review
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- Cancer histone mutations impact protein binding and DNA repair with possible links to genomic instability.Nucleic acids research · 2025Article
- Role of epigenetics in paediatric cancer pathogenesis & drug resistance.British journal of cancer · 2025Review
- Cancer epigenetic therapy: recent advances, challenges, and emerging opportunities.Epigenomics · 2025Review
- The H3.3K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.Molecular cell · 2024Article
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- The H3.3 K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.bioRxiv : the preprint server for biology · 2023Article
- SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters.Nature communications · 2022Article
- Oncohistones: Hijacking the histone code.Annual review of cancer biology · 2022Article
- Structure, Activity and Function of the NSD3 Protein Lysine Methyltransferase.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone H3.3K36M mutation, identified in over 90% of chondroblastoma cases, reprograms the H3K36 methylation landscape and gene expression to promote tumorigenesis. However, it's still unclear how the H3K36M mutation preferentially occurs in the histone H3 variant H3.3 in chondroblastomas. Here, we report that H3.3K36M-, but not H3.1K36M-, mutant cells showed increased colony formation ability and differentiation defects. H3K36 methylations and enhancers were reprogrammed to different status in H3.3K36M- and H3.1K36M-mutant cells. The reprogramming of H3K36 methylation and enhancers was depended on the specific loci at which H3.3K36M and H3.1K36M were incorporated. Moreover, targeting H3K36M-mutant proteins to the chromatin inhibited the H3K36 methylation locally. Taken together, these results highlight the roles of the chromatic localization of H3.3K36M-mutant protein in the reprogramming of the epigenome and the subsequent induction of tumorigenesis, and shed light on the molecular mechanisms by which the H3K36M mutation mainly occurs in histone H3.3 in chondroblastomas.
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