ArticleOncogene2016
ZNF281 contributes to the DNA damage response by controlling the expression of XRCC2 and XRCC4.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
33 citing papers in PubMed, 41 citations in OpenAlex.
- Advanced gene editing technologies for oncology mechanisms, applications, and clinical implementation.Cancer gene therapy · 2026Review
- Identification of gene conversion events in horse IGHV suggests preferential hotspots for diversification.Immunogenetics · 2026Article
- O-GlcNAcylation of XRCC4 controls its stability and confers resistance to DNA double-strand break damage in cancer cells.Cell death & disease · 2026Article
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Identification and validation of the role of ZNF281 in 5-fluorouracil chemotherapy of gastric cancer.Journal of cancer research and clinical oncology · 2024Article
- Zinc finger proteins: guardians of genome stability.Frontiers in cell and developmental biology · 2024Review
- Inhibition of the transcription factor ZNF281 by SUFU to suppress tumor cell migration.Cell death and differentiation · 2023Article
- ZNF281 drives hepatocyte senescence in alcoholic liver disease by reducing HK2-stabilized PINK1/Parkin-mediated mitophagy.Cell proliferation · 2023Article
- Expression of ZNF281 in colorectal cancer correlates with response to radiotherapy and survival.Annals of medicine · 2023Article
- ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis.International journal of molecular sciences · 2022Article
- ZFP281-BRCA2 prevents R-loop accumulation during DNA replication.Nature communications · 2022Article
- Circulating Tumor Cells in Breast Cancer Patients: A Balancing Act between Stemness, EMT Features and DNA Damage Responses.Cancers · 2022Review
- Impact of the interplay between stemness features, p53 and pol iota on replication pathway choices.Nucleic acids research · 2021Article
- Article
- Constructing and validating a diagnostic nomogram for multiple sclerosis via bioinformatic analysis.3 Biotech · 2021Article
- ZNF281-miR-543 Feedback Loop Regulates Transforming Growth Factor-β-Induced Breast Cancer Metastasis.Molecular therapy. Nucleic acids · 2020Article
- From single gene analysis to single cell profiling: a new era for precision medicine.Journal of experimental & clinical cancer research : CR · 2020Article
- ZNF281/Zfp281 is a target of miR-1 and counteracts muscle differentiation.Molecular oncology · 2020Article
- Interactome of vertebrate GAF/ThPOK reveals its diverse functions in gene regulation and DNA repair.Journal of biosciences · 2020Article
- Cell death in cancer in the era of precision medicine.Genes and immunity · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
ZNF281 is a zinc-finger factor involved in the control of cellular stemness and epithelial-mesenchymal transition (EMT). Here, we report that ZNF281 expression increased after genotoxic stress caused by DNA-damaging drugs. Comet assays demonstrated that DNA repair was delayed in cells silenced for the expression of ZNF281 and treated with etoposide. Furthermore, the expression of 10 DNA damage response genes was downregulated in cells treated with etoposide and silenced for ZNF281. In line with this finding, XRCC2 and XRCC4, two genes that take part in homologous recombination and non-homologous end joining, respectively, were transcriptionally activated by ZNF281 through a DNA-binding-dependent mechanism, as demonstrated by luciferase assays and Chromatin crosslinking ImmunoPrecipitation experiments. c-Myc, which also binds to the promoters of XRCC2 and XRCC4, was unable to promote their transcription or to modify ZNF281 activity. Of interest, bioinformatic analysis of 1971 breast cancer patients disclosed a significant correlation between the expression of ZNF281 and that of XRCC2. In summary, our data highlight, for the first time, the involvement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
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.