ArticleOncogene2001
Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 114 citations in OpenAlex.
- Cryogenic Gas-Phase Infrared Ion Spectroscopy of Ultraviolet-Induced Nucleotide Photoproducts.Analytical chemistry · 2025Article
- Medicinal evaluation and molecular docking study of osajin as an anti-inflammatory, antioxidant, and antiapoptotic agent against sepsis-associated acute kidney injury in rats.Renal failure · 2024Article
- The Role of Endoplasmic Reticulum Stress on Reducing Recombinant Protein Production in Mammalian Cells.Biochemical engineering journal · 2024Article
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- Protein expression of nucleolar protein 12 in the retina and its implication in protection of retina from UV irradiation damage.Cell death discovery · 2024Article
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- Analysis of Radiation Toxicity in Mammalian Cells Stably Transduced with MitochondrialInternational journal of molecular sciences · 2023Article
- Fast relaxing red and near-IR switchable azobenzenes with chalcogen and halogen substituents: periodic trends, tuneable thermal half-lives and chalcogen bonding.Chemical science · 2022Article
- Fucoidan/UVC Combined Treatment Exerts Preferential Antiproliferation in Oral Cancer Cells but Not Normal Cells.Antioxidants (Basel, Switzerland) · 2022Article
- 222-Nanometer Far-UVC Exposure Results in DNA Damage and Transcriptional Changes to Mammalian Cells.International journal of molecular sciences · 2022Article
- Combined Treatment of Nitrated [6,6,6]Tricycles Derivative (SK2)/Ultraviolet C Highly Inhibits Proliferation in Oral Cancer Cells In Vitro.Biomedicines · 2022Article
- Astaxanthin Protects Ultraviolet B-Induced Oxidative Stress and Apoptosis in Human Keratinocytes via Intrinsic Apoptotic Pathway.Annals of dermatology · 2022Article
- Combined Treatment with Cryptocaryone and Ultraviolet C Promotes Antiproliferation and Apoptosis of Oral Cancer Cells.International journal of molecular sciences · 2022Article
- Modulation of ERCC1-XPF Heterodimerization InhibitionFrontiers in oncology · 2022Article
- PARP-1 Is a Potential Marker of Retinal Photooxidation and a Key Signal Regulator in Retinal Light Injury.Oxidative medicine and cellular longevity · 2022Review
- Low Dose Combined Treatment with Ultraviolet-C and Withaferin a Enhances Selective Killing of Oral Cancer Cells.Antioxidants (Basel, Switzerland) · 2020Article
- Integrated, multicohort analysis reveals unified signature of systemic lupus erythematosus.JCI insight · 2020Article
- The Major Tegument Protein of Bovine Herpesvirus 1, VP8, Interacts with DNA Damage Response Proteins and Induces Apoptosis.Journal of virology · 2018Article
- Article
- Autophagy in UV Damage Response.Photochemistry and photobiology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. The expression of other members of the Bcl-2 family such as Bax, Bcl-x(L) and Bak were not affected. Bcl-2 decline is causally involved in UV-C induced apoptosis since overexpression of Bcl-2 protected NER deficient cells against apoptosis. We also demonstrate that caspase-8, caspase-9 and caspase-3 are activated and PARP is cleaved in response to unrepaired UV-C induced DNA damage. Caspase-8 activation occurred independently of CD95 receptor activation since CD95R/FasR and CD95L/FasL were not altered in expression, and transfection of transdominant negative FADD failed to block apoptosis. Overall, the data demonstrate that UV-C induced non-repaired DNA damage triggers apoptosis in NER deficient fibroblasts involving components of the intrinsic mitochondrial damage pathway.
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