ArticleNature structural & molecular biology2025
Super-silencer perturbation by EZH2 and REST inhibition leads to large loss of chromatin interactions and reduction in cancer growth.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Characterization of Protein Co-Localization and Histone Modifications at Enhancers Anchored in Chromatin Loops.Biology · 2026Article
- The Encyclopedia of DNA Elements.bioRxiv : the preprint server for biology · 2026Article
- Prolactin-Releasing Hormone Receptor (PRLHR) enhances radiosensitivity and exacerbates DNA damage in glioblastoma post-irradiation by inhibiting Y-box-binding protein-1 (YBX1) nuclear translocation: a novel perspective on precision radiotherapy.Molecular biomedicine · 2026Article
- Article
- Integrated analysis of the blood metallome and DNA methylation, gene expression, and protein levels of immune-associated genes in residents from mining region.Environmental geochemistry and health · 2026Article
- Targeting the 3D genome by anthracyclines for chemotherapeutic effects.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Super-silencers are crucial for development and carcinogenesis in B cells.Nature communications · 2025Article
- GSK343, an inhibitor of EZH2, prevents acquired cisplatin resistance in bladder cancer.Molecular genetics and genomics : MGG · 2025Article
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Authors and funding
20 authors.
Funding
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Abstract
Human silencers have been shown to regulate developmental gene expression. However, the functional importance of human silencers needs to be elucidated, such as whether they can form 'super-silencers' and whether they are linked to cancer progression. Here, we show two silencer components of the FGF18 gene can cooperate through compensatory chromatin interactions to form a super-silencer. Double knockout of two silencers exhibited synergistic upregulation of FGF18 expression and changes in cell identity. To perturb the super-silencers, we applied combinational treatment of an enhancer of zeste homolog 2 inhibitor GSK343, and a repressor element 1-silencing transcription factor inhibitor, X5050 ('GR'). Interestingly, GR led to severe loss of topologically associated domains and loops, which were associated with reduced CTCF and TOP2A mRNA levels. Moreover, GR synergistically upregulated super-silencer-controlled genes related to cell cycle, apoptosis and DNA damage, leading to anticancer effects in vivo. Overall, our data demonstrated a super-silencer example and showed that GR can disrupt super-silencers, potentially leading to cancer ablation.
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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.