ArticleDevelopmental cell2024
Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis.
Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Histone tail mutants: versatile tools for decoding chromatin, development, and disease.Trends in genetics : TIG · 2026Review
- Epigenetic Regulation of Sebaceous and Meibomian Glands: From Development to Disease.Biomedicines · 2026Review
- NSD2 upregulation is driven by high-risk HPV E6/E7 and disrupts epithelial differentiation in HPV-associated head and neck cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- H3K36 Methylation as a Guardian of Epigenome Integrity.Nature communications · 2025Article
- In vivo CRISPR screening reveals epigenetic regulators of hepatobiliary plasticity.Genes & development · 2025Article
- Targeting Epigenetic Dysregulations in Head and Neck Squamous Cell Carcinoma.Journal of dental research · 2025Review
- H3K36 methylation regulates cell plasticity and regeneration in the intestinal epithelium.Nature cell biology · 2025Article
- The H3.3K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.Molecular cell · 2024Article
- Genetic Tools for Cell Lineage Tracing and Profiling Developmental Trajectories in the Skin.The Journal of investigative dermatology · 2024Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Chromatin organization is essential for maintaining cell-fate trajectories and developmental programs. Here, we find that disruption of H3K36 methylation dramatically impairs normal epithelial differentiation and development, which promotes increased cellular plasticity and enrichment of alternative cell fates. Specifically, we observe a striking increase in the aberrant generation of excessive epithelial glandular tissues, including hypertrophic salivary, sebaceous, and meibomian glands, as well as enhanced squamous tumorigenesis. These phenotypic and gene expression manifestations are associated with loss of H3K36me2 and rewiring of repressive H3K27me3, changes we also observe in human patients with glandular hyperplasia. Collectively, these results have identified a critical role for H3K36 methylation in both in vivo epithelial cell-fate decisions and the prevention of squamous carcinogenesis and suggest that H3K36 methylation modulation may offer new avenues for the treatment of numerous common disorders driven by altered glandular function, which collectively affect large segments of the human population.
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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.