ArticleThe Journal of biological chemistry2011
Distinct roles of Ape1 protein in the repair of DNA damage induced by ionizing radiation or bleomycin.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 70 citations in OpenAlex.
- Functional Profiling of DNA Repair Pathways in Lung Cancer Patients Uncovers Radiotherapy-Induced and Cancer-Associated Alterations in Oxidative Lesion Repair.medRxiv : the preprint server for health sciences · 2026Article
- High APEX1 Expression Facilitates Osteosarcoma Cell Proliferation.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Deciphering repair pathways of clustered DNA damage in human TK6 cells: insights from atomic force microscopy direct visualization.Nucleic acids research · 2025Article
- Cosmic Ionizing Radiation: A DNA Damaging Agent That May Underly Excess Cancer in Flight Crews.International journal of molecular sciences · 2024Review
- Copy Number Variation That Influences the Ionizing Radiation Sensitivity of Oral Squamous Cell Carcinoma.Cells · 2023Article
- A specific dispiropiperazine derivative that arrests cell cycle, induces apoptosis, necrosis and DNA damage.Scientific reports · 2023Article
- Review
- Characterizing inhibitors of human AP endonuclease 1.PloS one · 2023Article
- Knockout and Inhibition of Ape1: Roles of Ape1 in Base Excision DNA Repair and Modulation of Gene Expression.Antioxidants (Basel, Switzerland) · 2022Article
- DNA Damage Clustering after Ionizing Radiation and Consequences in the Processing of Chromatin Breaks.Molecules (Basel, Switzerland) · 2022Review
- Small Interfering RNA for Gliomas Treatment: Overcoming Hurdles in Delivery.Frontiers in cell and developmental biology · 2022Review
- Mild phenotype of knockouts of the major apurinic/apyrimidinic endonuclease APEX1 in a non-cancer human cell line.PloS one · 2021Article
- Non-muscle invasive bladder cancer tissues have increased base excision repair capacity.Scientific reports · 2020Article
- Prion protein deficiency impairs hematopoietic stem cell determination and sensitizes myeloid progenitors to irradiation.Haematologica · 2020Article
- Functions of the major abasic endonuclease (APE1) in cell viability and genotoxin resistance.Mutagenesis · 2020Review
- Review
- Human DNA Telomeres in Presence of Oxidative Lesions: The Crucial Role of Electrostatic Interactions on the Stability of Guanine Quadruplexes.Antioxidants (Basel, Switzerland) · 2019Article
- The genome-wide sequence preference of ionising radiation-induced cleavage in human DNA.Molecular biology reports · 2019Article
- Phosphoglycolate has profound metabolic effects but most likely no role in a metabolic DNA response in cancer cell lines.The Biochemical journal · 2019Article
- Nanoparticle-mediated knockdown of DNA repair sensitizes cells to radiotherapy and extends survival in a genetic mouse model of glioblastoma.Nanomedicine : nanotechnology, biology, and medicine · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Ionizing radiation (IR) and bleomycin (BLM) are used to treat various types of cancers. Both agents generate cytotoxic double strand breaks (DSB) and abasic (apurinic/apyrimidinic (AP)) sites in DNA. The human AP endonuclease Ape1 acts on abasic or 3'-blocking DNA lesions such as those generated by IR or BLM. We examined the effect of siRNA-mediated Ape1 suppression on DNA repair and cellular resistance to IR or BLM in human B-lymphoblastoid TK6 cells and HCT116 colon tumor cells. Partial Ape1 deficiency (∼30% of normal levels) sensitized cells more dramatically to BLM than to IR cytotoxicity. In both cases, expression of the unrelated yeast AP endonuclease, Apn1, largely restored resistance. Ape1 deficiency increased DNA AP site accumulation due to IR treatment but reduced the number of DSB. In contrast, for BLM, there were more DSB under Ape1 deficiency, with little change in the accumulation of AP sites. Although the role of Ape1 in generating DSB was greater for IR, the enzyme facilitated removal of AP sites, which may mitigate the cytotoxic effects of IR. In contrast, BLM generates scattered AP sites, and the DSB have 3'-phosphoglycolate termini that require Ape1 processing. These DSB persist under Ape1 deficiency. Apoptosis induced by BLM (but not by IR) under Ape1 deficiency was partially p53-dependent, more dramatically in TK6 than HCT116 cells. Thus, Ape1 suppression or inhibition may be a more efficacious adjuvant for BLM than for IR cancer therapy, particularly for tumors with a functional p53 pathway.
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