ArticleAlcoholism, clinical and experimental research2011
Alcohol metabolism in human cells causes DNA damage and activates the Fanconi anemia-breast cancer susceptibility (FA-BRCA) DNA damage response network.
Article in Alcoholism, clinical and experimental research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Alcohol consumption and cancer progression: Mechanistic insights, immune dysregulation, and public health implications.Translational oncology · 2026Review
- Connecting the dots: investigating the link between environmental, genetic, and epigenetic influences in metabolomic alterations in oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Review
- Candidiasis in breast cancer: Tumor progression or not?Iranian journal of basic medical sciences · 2024Review
- Ethanol induces replication fork stalling and membrane stress in immortalized laryngeal cells.iScience · 2023Article
- Alcohol and vascular endothelial function: Biphasic effect highlights the importance of dose.Alcohol, clinical & experimental research · 2023Article
- FANCD2 limits acetaldehyde-induced genomic instability during DNA replication in esophageal keratinocytes.Molecular oncology · 2021Article
- The role of ALDH2 in tumorigenesis and tumor progression: Targeting ALDH2 as a potential cancer treatment.Acta pharmaceutica Sinica. B · 2021Review
- Formation and repair of unavoidable, endogenous interstrand cross-links in cellular DNA.DNA repair · 2021Review
- Prevalence and associated factors of baseline anemia among cervical cancer patients in Tikur Anbesa Specialized Hospital, Ethiopia.BMC women's health · 2021Article
- Interplay between base excision repair protein XRCC1 and ALDH2 predicts overall survival in lung and liver cancer patients.Cellular oncology (Dordrecht, Netherlands) · 2018Article
- Ethanol potentiates the genotoxicity of the food-derived mammary carcinogen PhIP in human estrogen receptor-positive mammary cells: mechanistic support for lifestyle factors (cooked red meat and ethanol) associated with mammary cancer.Archives of toxicology · 2018Article
- Formation and repair of DNA-protein crosslink damage.Science China. Life sciences · 2017Review
- Molecular Mechanisms of Acetaldehyde-Mediated Carcinogenesis in Squamous Epithelium.International journal of molecular sciences · 2017Review
- Genetic controls of DNA damage avoidance in response to acetaldehyde in fission yeast.Cell cycle (Georgetown, Tex.) · 2017Article
- p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells.PloS one · 2017Article
- Aldehyde dehydrogenase 2 in aplastic anemia, Fanconi anemia and hematopoietic stem cells.Molecular genetics and metabolism · 2016Review
- Addiction to Runx1 is partially attenuated by loss of p53 in the Eµ-Myc lymphoma model.Oncotarget · 2016Article
- A novel role for non-ubiquitinated FANCD2 in response to hydroxyurea-induced DNA damage.Oncogene · 2016Article
- Article
- Reduced FANCD2 influences spontaneous SCE and RAD51 foci formation in uveal melanoma and Fanconi anaemia.Oncogene · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe recently reported that exposure of human cells in vitro to acetaldehyde resulted in the activation of the Fanconi anemia-breast cancer susceptibility (FA-BRCA) DNA damage response network.
methodsTo determine whether intracellular generation of acetaldehyde from ethanol metabolism can cause DNA damage and activate the FA-BRCA network, we engineered HeLa cells to metabolize alcohol by expression of human alcohol dehydrogenase (ADH) 1B.
resultsIncubation of HeLa-ADH1B cells with ethanol (20 mM) resulted in acetaldehyde accumulation in the media, which was prevented by co-incubation with 4-methyl pyrazole (4-MP), a specific inhibitor of ADH. Ethanol treatment of HeLa-ADH1B cells produced a 4-fold increase in the acetaldehyde-DNA adduct and N(2)-ethylidene-dGuo and also resulted in the activation of the FA-BRCA DNA damage response network, as indicated by a monoubiquitination of FANCD2 and phosphorylation of BRCA1. Ser 1524 was identified as 1 site of BRCA1 phosphorylation. The increased levels of DNA adducts, FANCD2 monoubiquitination, and BRCA1 phosphorylation were all blocked by 4-MP, indicating that acetaldehyde, rather than ethanol itself, was responsible for all 3 responses. Importantly, the ethanol concentration we used is within the range that can be attained in the human body during social drinking.
conclusionsOur results indicate that intracellular metabolism of ethanol to acetaldehyde results in DNA damage, which activates the FA-BRCA DNA damage response network.
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