ArticleNucleic acids research2021
Replication catastrophe induced by cyclic hypoxia leads to increased APOBEC3B activity.
Article in Nucleic acids research, 2021. 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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Who cites it
21 citing papers in PubMed.
- Tumour hypoxia in clinical oncology: imaging, therapeutic strategies, and translational challenges.Clinical and translational radiation oncology · 2027Review
- HIF-1-regulated TPM3 links hypoxia to motility and invasion beyond the hypoxic fraction in triple-negative breast cancer.NPJ breast cancer · 2026Article
- Reprogramming tumor immunity through APOBEC3s-mediated mutagenesis: from genome instability to immune checkpoint interactions.Frontiers in immunology · 2026Review
- Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025Review
- Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3B.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Phosphorescence-basediScience · 2025Article
- Tumour hypoxia in driving genomic instability and tumour evolution.Nature reviews. Cancer · 2025Review
- Engineered hypoxia-responsive albumin nanoparticles mediating mitophagy regulation for cancer therapy.Nature communications · 2025Article
- Characterising Cancer Cell Responses to Cyclic Hypoxia Using Mathematical Modelling.Bulletin of mathematical biology · 2024Article
- Apolipoprotein-B mRNA-editing complex 3B could be a new potential therapeutic target in endometriosis.Scientific reports · 2024Article
- Hypoxia promotes histone H3K9 lactylation to enhanceiScience · 2024Article
- APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors.Cell death & disease · 2023Article
- APOBEC3B stratifies ovarian clear cell carcinoma with distinct immunophenotype and prognosis.British journal of cancer · 2023Article
- Review
- Claspin-Dependent and -Independent Chk1 Activation by a Panel of Biological Stresses.Biomolecules · 2023Article
- Understanding human aging and the fundamental cell signaling link in age-related diseases: the middle-aging hypovascularity hypoxia hypothesis.Frontiers in aging · 2023Article
- Modeling Preclinical Cancer Studies under Physioxia to Enhance Clinical Translation.Cancer research · 2022Review
- Identification of natural product 3, 5-diiodotyrosine as APOBEC3B inhibitor to prevent somatic mutation accumulation and cancer progression.Journal for immunotherapy of cancer · 2022Article
- The impact of macrophages on endothelial cells is potentiated by cycling hypoxia: Enhanced tumor inflammation and metastasis.Frontiers in oncology · 2022Article
- The Effect of Hypoxia and Hypoxia-Associated Pathways in the Regulation of Antitumor Response: Friends or Foes?Frontiers in immunology · 2022Review
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Authors and funding
8 authors.
Funding
Abstract
Tumor heterogeneity includes variable and fluctuating oxygen concentrations, which result in the accumulation of hypoxic regions in most solid tumors. Tumor hypoxia leads to increased therapy resistance and has been linked to genomic instability. Here, we tested the hypothesis that exposure to levels of hypoxia that cause replication stress could increase APOBEC activity and the accumulation of APOBEC-mediated mutations. APOBEC-dependent mutational signatures have been well-characterized, although the physiological conditions which underpin them have not been described. We demonstrate that fluctuating/cyclic hypoxic conditions which lead to replication catastrophe induce the expression and activity of APOBEC3B. In contrast, stable/chronic hypoxic conditions which induce replication stress in the absence of DNA damage are not sufficient to induce APOBEC3B. Most importantly, the number of APOBEC-mediated mutations in patient tumors correlated with a hypoxia signature. Together, our data support the conclusion that hypoxia-induced replication catastrophe drives genomic instability in tumors, specifically through increasing the activity of APOBEC3B.
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