ArticleScientific reports2017
Ape1 guides DNA repair pathway choice that is associated with drug tolerance in glioblastoma.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Selenium-modified graphene oxide: A tri-dimensional study of its cytotoxicity and developmental effects.Materials today. Bio · 2026Article
- Contrasting roles of APE1 and APE2 in genome maintenance, cancer development, and therapeutic targeting.NAR cancer · 2025Review
- ATG conjugation-dependent/independent mechanisms underlie lysosomal stress-induced TFEB regulation.The Journal of cell biology · 2025Article
- Teniposide Triggers DNA Repair Inhibition by Binding and Ubiquitination of Apurinic/Apyrimidinic Endonuclease 1 to Boost Oxidative DNA Damage for Lung Cancer Destruction.ACS pharmacology & translational science · 2025Article
- Explainable AI-driven prediction of APE1 inhibitors: enhancing cancer therapy with machine learning models and feature importance analysis.Molecular diversity · 2025Article
- TheInternational journal of molecular sciences · 2024Article
- AUF1 Recognizes 8-Oxo-Guanosine Embedded in DNA and Stimulates APE1 Endoribonuclease Activity.Antioxidants & redox signaling · 2023Article
- Antibody Profiling and In Silico Functional Analysis of Differentially Reactive Antibody Signatures of Glioblastomas and Meningiomas.International journal of molecular sciences · 2023Article
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Targets for Renal Carcinoma Growth Control Identified by Screening FOXD1 Cell Proliferation Pathways.Cancers · 2022Article
- The impact of rare germline variants on human somatic mutation processes.Nature communications · 2022Article
- SRPX Emerges as a Potential Tumor Marker in the Extracellular Vesicles of Glioblastoma.Cancers · 2022Article
- Article
- APE1 distinguishes DNA substrates in exonucleolytic cleavage by induced space-filling.Nature communications · 2021Article
- DNA alkylation lesion repair: outcomes and implications in cancer chemotherapy.Journal of Zhejiang University. Science. B · 2021Review
- Deficiency of Ku Induces Host Cell Exploitation in Human Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- Understanding APE1 cellular functions by the structural preference of exonuclease activities.Computational and structural biotechnology journal · 2021Review
- Review
- Prion protein deficiency impairs hematopoietic stem cell determination and sensitizes myeloid progenitors to irradiation.Haematologica · 2020Article
- Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Ape1 is the major apurinic/apyrimidinic (AP) endonuclease activity in mammalian cells, and a key factor in base-excision repair of DNA. High expression or aberrant subcellular distribution of Ape1 has been detected in many cancer types, correlated with drug response, tumor prognosis, or patient survival. Here we present evidence that Ape1 facilitates BRCA1-mediated homologous recombination repair (HR), while counteracting error-prone non-homologous end joining of DNA double-strand breaks. Furthermore, Ape1, coordinated with checkpoint kinase Chk2, regulates drug response of glioblastoma cells. Suppression of Ape1/Chk2 signaling in glioblastoma cells facilitates alternative means of damage site recruitment of HR proteins as part of a genomic defense system. Through targeting "HR-addicted" temozolomide-resistant glioblastoma cells via a chemical inhibitor of Rad51, we demonstrated that targeting HR is a promising strategy for glioblastoma therapy. Our study uncovers a critical role for Ape1 in DNA repair pathway choice, and provides a mechanistic understanding of DNA repair-supported chemoresistance in glioblastoma cells.
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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.