ArticleOxidative medicine and cellular longevity2016
Abnormal Expressions of DNA Glycosylase Genes NEIL1, NEIL2, and NEIL3 Are Associated with Somatic Mutation Loads in Human Cancer.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 55 citations in OpenAlex.
- Genetic associations with longevity in a Calabrian cohort: an exploratory genome-wide study.GeroScience · 2026Article
- Identification of tumor-associated antigens with multi-cancer therapeutic potential.Frontiers in immunology · 2026Article
- Dysregulated mitochondrial homeostasis and DNA repair in the progression from colon adenoma to cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- FOXM1 transcriptionally activates NEIL3 to inhibit ferroptosis in lung adenocarcinoma cells.Journal of clinical biochemistry and nutrition · 2025Article
- Identification and validation of NEIL2 as a prognostic biomarker and potential therapeutic target in cervical cancer.Discover oncology · 2025Article
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- E-cigarettes increase the risk of adenoma formation in murine colorectal cancer model.Archives of toxicology · 2025Article
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- E-cigarettes increase the risk of adenoma formation in murine colorectal cancer model.bioRxiv : the preprint server for biology · 2024Article
- Review
- Functional roles and cancer variants of the bifunctional glycosylase NEIL2.Environmental and molecular mutagenesis · 2024Review
- [Overexpression of Nei endonuclease VIII-like protein 3 in hepatocellular carcinoma indicates increased levels of immune infiltration and an unfavorable prognosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- The Curcumin Analog PAC Is a Potential Solution for the Treatment of Triple-Negative Breast Cancer by Modulating the Gene Expression of DNA Repair Pathways.International journal of molecular sciences · 2023Article
- The effects of altered DNA damage repair genes on mutational processes and immune cell infiltration in esophageal squamous cell carcinoma.Cancer medicine · 2023Article
- NEIL3-mediated proteasomal degradation facilitates the repair of cisplatin-induced DNA damage in human cells.Scientific reports · 2023Article
- Article
- Biological Functions of the DNA Glycosylase NEIL3 and Its Role in Disease Progression Including Cancer.Cancers · 2022Review
- Mono- and biallelic germline variants of DNA glycosylase genes in colon adenomatous polyposis families from two continents.Frontiers in oncology · 2022Article
- Construction of Bone Metastasis-Specific Regulation Network Based on Prognostic Stemness-Related Signatures in Prostate Cancer.Disease markers · 2022Article
- Identification of DNA Damage Repair-Associated Prognostic Biomarkers for Prostate Cancer Using Transcriptomic Data Analysis.International journal of molecular sciences · 2021Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of abnormalities in the DNA glycosylases NEIL1, NEIL2, and NEIL3 on human cancer have not been fully elucidated. In this paper, we found that the median somatic total mutation loads and the median somatic single nucleotide mutation loads exhibited significant inverse correlations with the median NEIL1 and NEIL2 expression levels and a significant positive correlation with the median NEIL3 expression level using data for 13 cancer types from the Cancer Genome Atlas (TCGA) database. A subset of the cancer types exhibited reduced NEIL1 and NEIL2 expressions and elevated NEIL3 expression, and such abnormal expressions of NEIL1, NEIL2, and NEIL3 were also significantly associated with the mutation loads in cancer. As a mechanism underlying the reduced expression of NEIL1 in cancer, the epigenetic silencing of NEIL1 through promoter hypermethylation was found. Finally, we investigated the reason why an elevated NEIL3 expression level was associated with an increased number of somatic mutations in cancer and found that NEIL3 expression was positively correlated with the expression of APOBEC3B, a potent inducer of mutations, in diverse cancers. These results suggested that the abnormal expressions of NEIL1, NEIL2, and NEIL3 are involved in cancer through their association with the somatic mutation load.
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