ArticleOncotarget2016
APE1 polymorphic variants cause persistent genomic stress and affect cancer cell proliferation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Impact of germline polymorphisms in genes regulating glucose uptake on positron emission tomography findings and outcome in diffuse large B-cell lymphoma: results from the PETAL trial.Journal of cancer research and clinical oncology · 2022Trial
- Contrasting roles of APE1 and APE2 in genome maintenance, cancer development, and therapeutic targeting.NAR cancer · 2025Review
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- Revisiting Two Decades of Research Focused on Targeting APE1 for Cancer Therapy: The Pros and Cons.Cells · 2023Review
- A Novel HypomorphicAntioxidants & redox signaling · 2023Article
- APE1/Ref-1 Role in Inflammation and Immune Response.Frontiers in immunology · 2022Review
- The multifunctional APE1 DNA repair-redox signaling protein as a drug target in human disease.Drug discovery today · 2021Review
- Sorafenib Resistance in Hepatocellular Carcinoma: The Relevance of Genetic Heterogeneity.Cancers · 2020Review
- Review
- Functions of the major abasic endonuclease (APE1) in cell viability and genotoxin resistance.Mutagenesis · 2020Review
- Architecture of The Human Ape1 Interactome Defines Novel Cancers Signatures.Scientific reports · 2020Article
- APE1 and NPM1 protect cancer cells from platinum compounds cytotoxicity and their expression pattern has a prognostic value in TNBC.Journal of experimental & clinical cancer research : CR · 2019Article
- Sequencing abasic sites in DNA at single-nucleotide resolution.Nature chemistry · 2019Article
- Human AP-endonuclease (Ape1) activity on telomeric G4 structures is modulated by acetylatable lysine residues in the N-terminal sequence.DNA repair · 2019Article
- APE1: A skilled nucleic acid surgeon.DNA repair · 2018Review
- The regulatory role of APE1 in epithelial-to-mesenchymal transition and in determining EGFR-TKI responsiveness in non-small-cell lung cancer.Cancer medicine · 2018Article
- DNA Repair Molecular Beacon assay: a platform for real-time functional analysis of cellular DNA repair capacity.Oncotarget · 2018Article
- Tumor-associated APE1 variant exhibits reduced complementation efficiency but does not promote cancer cell phenotypes.Environmental and molecular mutagenesis · 2017Article
- Base excision repair of oxidative DNA damage: from mechanism to disease.Frontiers in bioscience (Landmark edition) · 2017Review
- Exploiting the Ref-1-APE1 node in cancer signaling and other diseases: from bench to clinic.NPJ precision oncology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apurinic/apyrimidinic endonuclease 1 (APE1) is the main mammalian AP-endonuclease responsible for the repair of endogenous DNA damage through the base excision repair (BER) pathway. Molecular epidemiological studies have identified several genetic variants associated with human diseases, but a well-defined functional connection between mutations in APE1 and disease development is lacking. In order to understand the biological consequences of APE1 genetic mutations, we examined the molecular and cellular consequences of the selective expression of four non-synonymous APE1 variants (L104R, R237C, D148E and D283G) in human cells. We found that D283G, L104R and R237C variants have reduced endonuclease activity and impaired ability to associate with XRCC1 and DNA polymerase β, which are enzymes acting downstream of APE1 in the BER pathway. Complementation experiments performed in cells, where endogenous APE1 had been silenced by shRNA, showed that the expression of these variants resulted in increased phosphorylation of histone H2Ax and augmented levels of poly(ADP-ribosyl)ated (PAR) proteins. Persistent activation of DNA damage response markers was accompanied by growth defects likely due to combined apoptotic and autophagic processes. These phenotypes were observed in the absence of exogenous stressors, suggesting that chronic replication stress elicited by the BER defect may lead to a chronic activation of the DNA damage response. Hence, our data reinforce the concept that non-synonymous APE1 variants present in the human population may act as cancer susceptibility alleles.
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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.