ArticleCell cycle (Georgetown, Tex.)2012
Persistent DNA damage caused by low levels of mitomycin C induces irreversible cell senescence.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 61 citations in OpenAlex.
- The potential of gene therapy to rescue telomeric and extratelomeric defects in X-linked dyskeratosis congenita.Molecular therapy. Advances · 2026Article
- Surviving Fibroblasts After Treatment With Mitomycin C Exhibit SASP-Like Phenotype After Glaucoma Filtration Surgery.Aging cell · 2026Article
- Influence of Stress-Induced Senescence on the Secretome of Primary Mesenchymal Stromal Cells.Biomolecules · 2025Article
- Prodrug nanoplatform for triggering ferroptosis to eliminate senescent cells in age-associated pathologies.Nature communications · 2025Article
- Pre-Vascularized 3-Dimensional Skin Substitutes Promote Angiogenesis and Tissue Repair in a Murine Model of Refractory Skin Ulcers.Journal of functional biomaterials · 2025Article
- The Impact of Polyploid Giant Cancer Cells: The Root of Stress Resilience.Cancer science · 2025Review
- Metabolic Reprogramming of Urothelial Carcinoma-A Theragnostic Target for Betulinic Acid.International journal of molecular sciences · 2025Article
- Article
- Senescence-Associated Alterations in Matrisome of Mesenchymal Stem Cells.International journal of molecular sciences · 2024Article
- Regenerative Therapy for Corneal Scarring Disorders.Biomedicines · 2024Review
- Polyploid giant cancer cells: origin, possible pathways of formation, characteristics, and mechanisms of regulation.Frontiers in cell and developmental biology · 2024Review
- Dynamics of redox signaling in aging via autophagy, inflammation, and senescence.Biogerontology · 2023Review
- Mitochondrial Transport from Mesenchymal Stromal Cells to Chondrocytes Increases DNA Content and Proteoglycan DepositionCartilage · 2022Article
- A senolysis-based theragnostic prodrug strategy towards chronic renal failure.Chemical science · 2022Article
- Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2.JCI insight · 2022Article
- A novel in vitro 3D model of the human bone marrow to bridge the gap between in vitro and in vivo genotoxicity testing.Mutagenesis · 2022Article
- Confocal microscopy reveals alterations of thylakoids in Limnospira fusiformis during prophage induction.Protoplasma · 2021Article
- BET bromodomain inhibitors regulate keratinocyte plasticity.Nature chemical biology · 2021Article
- Safety and efficacy of combination of suberoylamilide hydroxyamic acid and mitomycin C in reducing pro-fibrotic changes in human corneal epithelial cells.Scientific reports · 2021Article
- Cell-Free Biological Approach for Corneal Stromal Wound Healing.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations of oncogenes and tumor suppressor genes which activate mTOR through several downstream signaling pathways are common to cancer. Activation of mTOR when combined with inhibition of cell cycle progression or DNA replication stress has previously been shown to promote cell senescence. In the present study, we examined the conditions under which human non-small cell lung carcinoma A549 cells can undergo senescence when treated with the DNA alkylating agent mitomycin C (MMC). While exposure of A549 cells to 0.1 or 0.5 µg/ml of MMC led to their arrest in S phase of the cell cycle and subsequent apoptosis, exposure to 0.01 or 0.02 µg/ml for 6 d resulted in induction of cell senescence and near total (0.01 µg/ml) or total (0.02 µg/ml) elimination of their reproductive potential. During exposure to these low concentrations of MMC, the cells demonstrated evidence of DNA replication stress manifested by expression of γH2AX, p21 (WAF1) and a very low level of EdU incorporation into DNA. The data are consistent with the notion that enduring DNA replication stress in cells known to have activated oncogenes leads to their senescence. It is reasonable to expect that tumors having constitutive activation of oncogenes triggering mTOR signaling may be particularly predisposed to undergoing senescence following prolonged treatment with low doses of DNA damaging drugs.
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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.