ArticleCell death & disease2014
Radiation induces senescence and a bystander effect through metabolic alterations.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 93 citations in OpenAlex.
- Low-Dose Ionizing Radiation and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Review of Recent Evidence and Future Research Directions Toward the Elucidation of a Metabolic, Immunologic, and Signaling Cascade.International journal of molecular sciences · 2026Review
- Neonatal hyperoxia promotes macrophage senescence and lung injury via a p38MAPK-dependent secretome.American journal of respiratory cell and molecular biology · 2026Article
- Postbiotics as Emerging Strategy Targeting Obesity- and Aging-Related Breast Cancer-Prospects in Prophylaxis and Therapy.Life (Basel, Switzerland) · 2026Review
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- The Implications of Radiotherapy-Induced Cellular Senescence for Cancer Treatment and Tumor Microenvironment Modulation.International journal of biological sciences · 2026Review
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Senescent fibroblasts in aging and pulmonary fibrosis.Frontiers in aging · 2026Review
- Review
- Advanced glycation end products induce inflammaging in periodontal ligament fibroblasts through RAGE/AKT/mTOR/glycolysis pathway.Acta odontologica Scandinavica · 2025Article
- Radiation Promotes Acute and Chronic Damage to Adipose Tissue.International journal of molecular sciences · 2025Article
- Radiotherapy elicits immunogenic cell death and metabolic shifts in the tumor microenvironment: implications for immunotherapy.International journal of medical sciences · 2025Review
- uPAR Immuno-PET in Pancreatic Cancer, Aging, and Chemotherapy-Induced Senescence.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024Article
- Review
- Multiparametric identification of putative senescent cells in skeletal muscle via mass cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024Article
- Cellular senescence of renal tubular epithelial cells in acute kidney injury.Cell death discovery · 2024Review
- Therapy-induced senescence in breast cancer: an overview.Exploration of targeted anti-tumor therapy · 2024Review
- Targeting PDK2 rescues stress-induced impaired brain energy metabolism.Molecular psychiatry · 2023Article
- Irreversible cell cycle exit associated with senescence is mediated by constitutive MYC degradation.Cell reports · 2023Article
- Ultra-high dose-rate proton FLASH improves tumor control.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023Article
- Advances in PET imaging of cancer.Nature reviews. Cancer · 2023Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a state of irreversible growth arrest; however, the metabolic processes of senescent cells remain active. Our previous studies have shown that radiation induces senescence of human breast cancer cells that display low expression of securin, a protein involved in control of the metaphase-anaphase transition and anaphase onset. In this study, the protein expression profile of senescent cells was resolved by two-dimensional gel electrophoresis to investigate associated metabolic alterations. We found that radiation induced the expression and activation of glyceraldehyde-3-phosphate dehydrogenase that has an important role in glycolysis. The activity of lactate dehydrogenase A, which is involved in the conversion of pyruvate to lactate, the release of lactate and the acidification of the extracellular environment, was also induced. Inhibition of glycolysis by dichloroacetate attenuated radiation-induced senescence. In addition, radiation also induced activation of the 5'-adenosine monophosphate-activated protein kinase (AMPK) and nuclear factor kappa B (NF-κB) pathways to promote senescence. We also found that radiation increased the expression of monocarboxylate transporter 1 (MCT1) that facilitates the export of lactate into the extracellular environment. Inhibition of glycolysis or the AMPK/NF-κB signalling pathways reduced MCT1 expression and rescued the acidification of the extracellular environment. Interestingly, these metabolic-altering signalling pathways were also involved in radiation-induced invasion of the surrounding, non-irradiated breast cancer and normal endothelial cells. Taken together, radiation can induce the senescence of human breast cancer cells through metabolic alterations.
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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.