ArticleGenome research2017
Critical threshold levels of DNA methyltransferase 1 are required to maintain DNA methylation across the genome in human cancer cells.
Article in Genome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 90 citations in OpenAlex.
- Live-cell DNMT3A "catalysome" mapping using engineered methyl-transfer pathways.Nucleic acids research · 2026Article
- Reduced Maintenance DNA Methylation Thresholds Enable Sensitive Reporter Assays for UHRF1 and DNMT1 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structure-guided design of 7-azaindole DNMT1 inhibitors active against hypomethylating agent-resistant acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- UHRF1 drives hepatocellular carcinoma progression via epigenetic repression of SFMBT2.Scientific reports · 2026Article
- UHRF1 deficiency exacerbates intestinal inflammation by epigenetic modulation of NPY1R gene methylation.JCI insight · 2026Article
- Discovery of a Novel DNMT1 Inhibitor with Improved Efficacy in Treating β-Thalassemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Applications of CRISPR-Cas9 in mitigating cellular senescence and age-related disease progression.Clinical and experimental medicine · 2025Review
- Applications of CRISPR-Cas9 in mitigating cellular senescence and age-related disease progression.Clinical and experimental medicine · 2025Review
- DNA methylation protects cancer cells against senescence.Nature communications · 2025Article
- UHRF1 phase separation mediates stable inheritance of DNA methylation and promotes the proliferation of prostate cancer cells.Cell communication and signaling : CCS · 2025Article
- Defining ortholog-specific UHRF1 inhibition by STELLA for cancer therapy.Nature communications · 2025Article
- Review
- DNA Methylation in the Adaptive Response to Exercise.Sports medicine (Auckland, N.Z.) · 2024Review
- Current data and future perspectives on DNA methylation in ovarian cancer (Review).International journal of oncology · 2024Review
- DNMT3B splicing dysregulation mediated by SMCHD1 loss contributes to DUX4 overexpression and FSHD pathogenesis.Science advances · 2024Article
- Non-canonical functions of UHRF1 maintain DNA methylation homeostasis in cancer cells.Nature communications · 2024Article
- Tunable DNMT1 degradation reveals DNMT1/DNMT3B synergy in DNA methylation and genome organization.The Journal of cell biology · 2024Article
- The UHRF1 protein is a key regulator of retrotransposable elements and innate immune response to viral RNA in human cells.Epigenetics · 2023Article
- Mechanistic insights into UHRF1‑mediated DNA methylation by structure‑based functional clarification of UHRF1 domains (Review).Oncology letters · 2023Review
- UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma.Nature communications · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Reversing DNA methylation abnormalities and associated gene silencing, through inhibiting DNA methyltransferases (DNMTs) is an important potential cancer therapy paradigm. Maximizing this potential requires defining precisely how these enzymes maintain genome-wide, cancer-specific DNA methylation. To date, there is incomplete understanding of precisely how the three DNMTs, 1, 3A, and 3B, interact for maintaining DNA methylation abnormalities in cancer. By combining genetic and shRNA depletion strategies, we define not only a dominant role for DNA methyltransferase 1 (DNMT1) but also distinct roles of 3A and 3B in genome-wide DNA methylation maintenance. Lowering DNMT1 below a threshold level is required for maximal loss of DNA methylation at all genomic regions, including gene body and enhancer regions, and for maximally reversing abnormal promoter DNA hypermethylation and associated gene silencing to reexpress key genes. It is difficult to reach this threshold with patient-tolerable doses of current DNMT inhibitors (DNMTIs). We show that new approaches, like decreasing the DNMT targeting protein, UHRF1, can augment the DNA demethylation capacities of existing DNA methylation inhibitors for fully realizing their therapeutic potential.
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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.