ArticleOncotarget2016
Mitochondrial reactive oxygen species perturb AKT/cyclin D1 cell cycle signaling via oxidative inactivation of PP2A in lowdose irradiated human fibroblasts.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 66 citations in OpenAlex.
- Mechanistic Effects of Environmental and Medical Low-Dose Radiation Exposure of the Lung.Biomedicines · 2026Review
- Review
- Mitochondrial reactive oxygen species impact human fibroblast responses to protracted γ-ray exposures.International journal of radiation biology · 2024Article
- The DNA damage response to radiological imaging: from ROS and γH2AX foci induction to gene expression responses in vivo.Radiation and environmental biophysics · 2023Article
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
- NNAT is a novel mediator of oxidative stress that suppresses ER + breast cancer.Molecular medicine (Cambridge, Mass.) · 2023Article
- Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023Review
- Article
- Radiation affects glutathione redox reaction by reduced glutathione peroxidase activity in human fibroblasts.Journal of radiation research · 2022Article
- Review
- Review
- Pleiotropic and Potentially Beneficial Effects of Reactive Oxygen Species on the Intracellular Signaling Pathways in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2021Review
- The role of mitochondrial oxidative stress and the tumor microenvironment in radiation-related cancer.Journal of radiation research · 2021Review
- Mechanism of turnover or persistence of radiation-induced myofibroblast in vitro.Cell cycle (Georgetown, Tex.) · 2020Article
- Roles of Reactive Oxygen Species in Biological Behaviors of Prostate Cancer.BioMed research international · 2020Review
- Article
- Interplay between BMPs and Reactive Oxygen Species in Cell Signaling and Pathology.Biomolecules · 2019Review
- Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression.International journal of molecular sciences · 2019Review
- Senescent Hepatocytes in Decompensated Liver Show Reduced UPRCellular and molecular gastroenterology and hepatology · 2019Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we investigated the cellular response of normal human fibroblasts to repeated exposure to low-dose radiation. In contrast to acute single radiation, low-dose fractionated radiation (FR) with 0.01 Gy/fraction or 0.05 Gy/fraction for 31 days increased in mitochondrial mass, decreased cellular levels of the antioxidant glutathione and caused persistent accumulation of mitochondrial reactive oxygen species (ROS). Excess ROS promoted oxidative inactivation of protein phosphatase PP2A which in turn led to disruption of normal negative feed-back control of AKT/cyclin D1 signaling in cells treated with long-term FR. The resulting abnormal nuclear accumulation of cyclin D1 causes growth retardation, cellular senescence and genome instability in low-dose irradiated cells. Thus, loss of redox control and subsequently elevated levels of ROS perturb signal transduction as a result of oxidative stress. Our study highlights a specific role of mitochondrial ROS in perturbation of AKT/cyclin D1 cell cycle signaling after low-dose long-term FR. The antioxidants N-acetyl-L-cysteine, TEMPO and mitochondrial-targeted antioxidant Mito-TEMPO provided protection against the harmful cell cycle perturbations induced by low-dose long-term FR.
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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.