DNA breakage and cell cycle checkpoint abrogation induced by a therapeutic thiopurine and UVA radiation
Open accessAbstract
The frequency of squamous cell skin carcinoma in organ transplant patients is around 100-fold higher than normal. This dramatic example of therapy-related cancer reflects exposure to sunlight and to immunosuppressive drugs. Here, we show that the interaction between low doses of UVA, the major ultraviolet component of incident sunlight, and 6-TG, a UVA chromophore that is introduced into DNA by one of the most widely prescribed immunosuppressive drugs, causes DNA single- and double-strand breaks (DSB). S phase cells are particularly vulnerable to this DNA breakage and cells defective in rejoining of S-phase DSB are hypersensitive to the combination of low-dose UVA and DNA 6-TG. 6-TG/UVA-induced DNA lesions provoke canonical DNA damage responses involving activation of the ATM/Chk2 and ATR/Chk1 pathways and appropriate cell cycle checkpoints. Higher levels of photochemical DNA damage induce a proteasome-mediated degradation of Chk1 and checkpoint abrogation that is consistent with persistent unrepaired DNA damage. These findings indicate that the interaction between UVA and an immunosuppressant drug causes photochemical DNA lesions, including DNA breaks, and can compromise cell cycle checkpoints. These two properties could contribute to the high risk of sunlight-related skin cancer in long-term immunosuppressed patients.
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UVA activation of thiopurines causes inhibition of transcription and abrogation of cell-cycle checkpoints in cultured human cells through generation of DNA damage.
“An indication for the induction of the deleterious effects triggered by UVA activation of thiopurines was provided indirectly by the observed inhibition of transcription (207) and abrogation of cell-cycle checkpoints (208) in cultured human cells treated with thiopurine and UVA radiation through the generation of DNA damage.”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions<sup>†</sup> (2012) · cites this paper as [208]
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- Authors
- Brem, R., Li, F., Montaner, B., Reelfs, O., & Karran, P.
- Affiliations
- Cancer Research UK (GB)
- Guy's Hospital (GB)
- Corresponding author
- Karran, P
- Venue
- Oncogene
- Published
- 2010-05-03
- Volume
- 29
- Issue
- 27
- Pages
- 3953-3963
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC2901207
- OpenAlex
- W2061414242
- Cited by
- 42
- References
- 39
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 5 · 2016: 4 · 2015: 3 · 2014: 3 · 2013: 2 · 2012: 6
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Cancer Research UK (A3558, 11584)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- thiopurines, 6-thioguanine, UVA, DNA double-strand breaks, single-strand breaks, cell cycle checkpoints, immunosuppressants, transplant recipients, DNA photodamage, ATM-Chk2 pathway, ATR-Chk1 pathway, DNA damage response, S phase
- MeSH terms
- Checkpoint Kinase 1, Animals, Antineoplastic Agents, Cell Cycle, Cricetulus, DNA Repair, DNA Replication, Dose-Response Relationship, Radiation, Cricetinae, Humans, Protein Kinases, Thioguanine, Ultraviolet Rays, CHO Cells, HCT116 Cells, DNA Breaks, Double-Stranded, DNA Breaks, Single-Stranded, DNA Breaks, Photochemical Processes
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