ArticleNucleic acids research2018
Overexpression of the base excision repair NTHL1 glycosylase causes genomic instability and early cellular hallmarks of cancer.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- Functional impact of Nth like DNA glycosylase 1 on mitochondrial dynamics.Nucleic acids research · 2026Article
- Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.International journal of radiation biology · 2026Review
- Increased vulnerability of colorectal cancer models with high alkylation damage to NTHL1 inactivation.Scientific reports · 2026Article
- A monofunctional-like mutant of DNA glycosylase NTHL1 changes the dynamics of DNA repair during acute oxidative stress.The Journal of biological chemistry · 2026Article
- Identification of prognostic genes associated with mitochondria and macrophage polarization in prostate adenocarcinoma based on transcriptome and Mendelian randomization analysis.Discover oncology · 2025Article
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- Chemical Switching: A Concept Inspired by Strategies from Biocatalysis and Organocatalysis.Chembiochem : a European journal of chemical biology · 2025Review
- E-cigarettes increase the risk of adenoma formation in murine colorectal cancer model.Archives of toxicology · 2025Article
- The Ribonuclease ZC3H12A is required for self-inflicted DNA breaks after DNA damage in small cell lung cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Enhanced Sampling for Conformational Changes and Molecular Mechanisms of Human NTHL1.The journal of physical chemistry letters · 2024Article
- Human NTHL1 expression and subcellular distribution determines cisplatin sensitivity in human lung epithelial and non-small cell lung cancer cells.NAR cancer · 2024Article
- The causal nexus between diverse smoking statuses, potential therapeutic targets, and NSCLC: insights from Mendelian randomization and mediation analysis.Frontiers in oncology · 2024Article
- Review
- Article
- OGG1 contributes to hepatocellular carcinoma by promoting cell cycle-related protein expression and enhancing DNA oxidative damage repair in tumor cells.Journal of clinical laboratory analysis · 2022Article
- Wilms tumor reveals DNA repair gene hyperexpression is linked to lack of tumor immune infiltration.Journal for immunotherapy of cancer · 2022Article
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Hypermethylation ofEXCLI journal · 2022Article
- Caught in motion: human NTHL1 undergoes interdomain rearrangement necessary for catalysis.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Base excision repair (BER), which is initiated by DNA N-glycosylase proteins, is the frontline for repairing potentially mutagenic DNA base damage. The NTHL1 glycosylase, which excises DNA base damage caused by reactive oxygen species, is thought to be a tumor suppressor. However, in addition to NTHL1 loss-of-function mutations, our analysis of cancer genomic datasets reveals that NTHL1 frequently undergoes amplification or upregulation in some cancers. Whether NTHL1 overexpression could contribute to cancer phenotypes has not yet been explored. To address the functional consequences of NTHL1 overexpression, we employed transient overexpression. Both NTHL1 and a catalytically-dead NTHL1 (CATmut) induce DNA damage and genomic instability in non-transformed human bronchial epithelial cells (HBEC) when overexpressed. Strikingly, overexpression of either NTHL1 or CATmut causes replication stress signaling and a decrease in homologous recombination (HR). HBEC cells that overexpress NTHL1 or CATmut acquire the ability to grow in soft agar and exhibit loss of contact inhibition, suggesting that a mechanism independent of NTHL1 catalytic activity contributes to acquisition of cancer-related cellular phenotypes. We provide evidence that NTHL1 interacts with the multifunctional DNA repair protein XPG suggesting that interference with HR is a possible mechanism that contributes to acquisition of early cellular hallmarks of cancer.
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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.