ArticleOncotarget2016
Distinct biological effects of low-dose radiation on normal and cancerous human lung cells are mediated by ATM signaling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Advances in Radiotherapy for Neoadjuvant Therapy of Stage III Non-Small Cell Lung Cancer.Cancer science · 2026Review
- Mechanistic Effects of Environmental and Medical Low-Dose Radiation Exposure of the Lung.Biomedicines · 2026Review
- Differential regulation of radioadaptation by quercetin between human normal and cancer cells.Clinical and translational radiation oncology · 2026Article
- RPL29 as a radiotherapy-sensitive prognostic biomarker in multiple myeloma.World journal of surgical oncology · 2025Article
- 0.5 Gy confers resistance to a subsequent high dose of γ-rays by modulating HO-1/Nrf2 and apoptosis pathways.Scientific reports · 2025Article
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
- Therapeutic potential of low dose ionizing radiation against cancer, dementia, and diabetes: evidences from epidemiological, clinical, and preclinical studies.Molecular biology reports · 2023Review
- Low-dose radiation exaggerates HFD-induced metabolic dysfunction by gut microbiota through PA-PYCR1 axis.Communications biology · 2022Article
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
- Low dose radiation prevents doxorubicin-induced cardiotoxicity.Oncotarget · 2018Article
- Biological basis of radiation protection needs rejuvenation.International journal of radiation biology · 2017Review
- Effects of low-dose radiation on adaptive response in colon cancer stem cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Article
- Hormetic Response to Low-Dose Radiation: Focus on the Immune System and Its Clinical Implications.International journal of molecular sciences · 2017Review
- Research Progress on the Biological Effects of Low-Dose Radiation in China.Dose-response : a publication of International Hormesis SocietyArticle
- Reduction of Delayed Homologous Recombination by Induction of Radioadaptive Response in RaDR-GFP Mice (Yonezawa Effect): An Old Player With a New Role.Dose-response : a publication of International Hormesis SocietyArticle
- Changes in the Proliferation Rate, Clonogenicity, and Radiosensitivity of Cultured Cells During and After Continuous Low-Dose-Rate Irradiation.Dose-response : a publication of International Hormesis SocietyArticle
- Influence of Individual Radiosensitivity on the Hormesis Phenomenon: Toward a Mechanistic Explanation Based on the Nucleoshuttling of ATM Protein.Dose-response : a publication of International Hormesis SocietyReview
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low-dose radiation (LDR) induces hormesis and adaptive response in normal cells but not in cancer cells, suggesting its potential protection of normal tissue against damage induced by conventional radiotherapy. However, the underlying mechanisms are not well established. We addressed this in the present study by examining the role of the ataxia telangiectasia mutated (ATM) signaling pathway in response to LDR using A549 human lung adenocarcinoma cells and HBE135-E6E7 (HBE) normal lung epithelial cells. We found that LDR-activated ATM was the initiating event in hormesis and adaptive response to LDR in HBE cells. ATM activation increased the expression of CDK4/CDK6/cyclin D1 by activating the AKT/glycogen synthase kinase (GSK)-3β signaling pathway, which stimulated HBE cell proliferation. Activation of ATM/AKT/GSK-3β signaling also increased nuclear accumulation of nuclear factor erythroid 2-related factor 2, leading to increased expression of antioxidants, which mitigated cellular damage from excessive reactive oxygen species production induced by high-dose radiation. However, these effects were not observed in A549 cells. Thus, the failure to activate these pathways in A549 cells likely explains the difference between normal and cancer cells in terms of hormesis and adaptive response to LDR.
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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.