ArticleNature communications2019
Protein lysine 43 methylation by EZH1 promotes AML1-ETO transcriptional repression in leukemia.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 34 citations in OpenAlex.
- The RNA NCell death & disease · 2025Article
- CD133-Guided RNA Nanoparticle Delivery of FTO siRNA Impairs Leukemia Resistance to Tyrosine Kinase Inhibitor Therapy.RNA nanomed · 2025Article
- The RNA NResearch square · 2024Article
- Coordinated activation of DNMT3a and TET2 in cancer stem cell-like cells initiates and sustains drug resistance in hepatocellular carcinoma.Cancer cell international · 2024Article
- Article
- [Characteristics of N6-methyladenosine modification patterns in t(8;21) acute myeloid leukemia].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Article
- Transcriptome-Wide Analysis of RNA NFrontiers in genetics · 2022Article
- Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- Saikosaponin D exhibits anti-leukemic activity by targeting FTO/mTheranostics · 2021Article
Corrections and comments
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Authors and funding
28 authors at 6 institutions in 2 countries.
Funding
Abstract
The oncogenic fusion protein AML1-ETO retains the ability of AML1 to interact with the enhancer core DNA sequences, but blocks AML1-dependent transcription. Previous studies have shown that post-translational modification of AML1-ETO may play a role in its regulation. Here we report that AML1-ETO-positive patients, with high histone lysine methyltransferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. We find that EZH1 WD domain binds to the AML1-ETO NHR1 domain and methylates AML1-ETO at lysine 43 (Lys43). This requires the EZH1 SET domain, which augments AML1-ETO-dependent repression of tumor suppressor genes. Loss of Lys43 methylation by point mutation or domain deletion impairs AML1-ETO-repressive activity. These findings highlight the role of EZH1 in non-histone lysine methylation, indicating that cooperation between AML1-ETO and EZH1 and AML1-ETO site-specific lysine methylation promote AML1-ETO transcriptional repression in leukemia.
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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.