ArticleOncotarget2017
Non-homologous end joining induced alterations in DNA methylation: A source of permanent epigenetic change.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Hierarchies of resistance to DNA damage response inhibitors: from pathway restoration to replication stress tolerance.Experimental hematology & oncology · 2026Review
- Disruption of DNA methylation underpins the neuroinflammation induced by targeted CNS radiotherapy.Brain : a journal of neurology · 2025Article
- Somatic mutation as an explanation for epigenetic aging.Nature aging · 2025Article
- The DNA methylome of pediatric brain tumors appears shaped by structural variation and predicts survival.Nature communications · 2024Article
- Targeting shared pathways in tauopathies and age-related macular degeneration: implications for novel therapies.Frontiers in aging neuroscience · 2024Review
- Somatic mutation as an explanation for epigenetic aging.bioRxiv : the preprint server for biology · 2023Article
- Identification of a robust DNA methylation signature for Fanconi anemia.American journal of human genetics · 2023Article
- Alterations in the Epigenetic Machinery Associated with Prostate Cancer Health Disparities.Cancers · 2023Article
- Specific Methyl-CpG Configurations Define Cell Identity through Gene Expression Regulation.International journal of molecular sciences · 2023Article
- LncRNA HOTAIRM1 functions in DNA double-strand break repair via its association with DNA repair and mRNA surveillance factors.Nucleic acids research · 2023Article
- Inflammation and DNA damage: cause, effect or both.Nature reviews. Rheumatology · 2023Review
- DNA Repair Mechanisms, Protein Interactions and Therapeutic Targeting of the MRN Complex.Cancers · 2022Review
- Review
- Unraveling the functional role of DNA demethylation at specific promoters by targeted steric blockage of DNA methyltransferase with CRISPR/dCas9.Nature communications · 2021Article
- Epigenome Chaos: Stochastic and Deterministic DNA Methylation Events Drive Cancer Evolution.Cancers · 2021Review
- Article
- Tracing and tracking epiallele families in complex DNA populations.NAR genomics and bioinformatics · 2020Article
- Chromosome structural variation in tumorigenesis: mechanisms of formation and carcinogenesis.Epigenetics & chromatin · 2020Review
- Methylation of the Suppressor GeneBiomolecules · 2020Article
- Association of glomerular DNA damage and DNA methylation with one-year eGFR decline in IgA nephropathy.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 3 countries.
Funding
Abstract
In addition to genetic mutations, epigenetic revision plays a major role in the development and progression of cancer; specifically, inappropriate DNA methylation or demethylation of CpG residues may alter the expression of genes that promote tumorigenesis. We hypothesize that DNA repair, specifically the repair of DNA double strand breaks (DSB) by Non-Homologous End Joining (NHEJ) may play a role in this process. Using a GFP reporter system inserted into the genome of HeLa cells, we are able to induce targeted DNA damage that enables the cells, after successfully undergoing NHEJ repair, to express WT GFP. These GFP+ cells were segregated into two expression classes, one with robust expression (Bright) and the other with reduced expression (Dim). Using a DNA hypomethylating drug (AzadC) we demonstrated that the different GFP expression levels was due to differential methylation statuses of CpGs in regions on either side of the break site. Deep sequencing analysis of this area in sorted Bright and Dim populations revealed a collection of different epi-alleles that display patterns of DNA methylation following repair by NHEJ. These patterns differ between Bright and Dim cells which are hypo- and hypermethylated, respectively, and between the post-repair populations and the original, uncut cells. These data suggest that NHEJ repair facilitates a rewrite of the methylation landscape in repaired genes, elucidating a potential source for the altered methylation patterns seen in cancer cells, and understanding the mechanism by which this occurs could provide new therapeutic targets for preventing this process from contributing to tumorigenesis.
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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.