ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Polycyclic Aromatic Hydrocarbon-induced Pulmonary Carcinogenesis in Cytochrome P450 (CYP)1A1- and 1A2-Null Mice: Roles of CYP1A1 and CYP1A2.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 42 citations in OpenAlex.
- Interpretable Machine Learning to Understand Wildfire Toxicity: Bridging Chemicals, Omics, and Toxicological Outcomes via Symbolic Regression with Novel Feature Scoring.Chemical research in toxicology · 2026Article
- Polycyclic aromatic hydrocarbon exposure and depressive symptoms among middle-aged and older Chinese adults: a prospective cohort study using CHARLS data.BMC public health · 2026Article
- Integrated bioinformatics and molecular docking ıdentify CCNB1, CDK1, and CYP1A2 as therapeutic targets of phytochemicals in hepatocellular carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Discovery of flavonoids as potent inhibitors of CYP1A to alleviate cellular inflammation and oxidative stress induced by benzo[a]pyrene-induced high CYP1A expression.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Evaluation and Correlation of 17β-Estradiol in Blood and Estrogen Receptor α (ERα) and Estrogen Receptor β(ER β) in Tissue of Oral Squamous Cell Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- An epigenetic memory at the CYP1A gene in cancer-resistant, pollution-adapted killifish.Scientific reports · 2025Article
- The impact of the exposome on cytochrome P450-mediated drug metabolism.Frontiers in pharmacology · 2025Review
- An epigenetic memory at thebioRxiv : the preprint server for biology · 2024Article
- Attenuation of Polycyclic Aromatic Hydrocarbon (PAH)-Induced Carcinogenesis and Tumorigenesis by Omega-3 Fatty Acids in Mice In Vivo.International journal of molecular sciences · 2024Article
- Particulate polycyclic aromatic hydrocarbons in rural households burning solid fuels in Xuanwei County, Southwest China: occurrence, size distribution, and health risks.Environmental science and pollution research international · 2024Article
- Article
- Network pharmacology-based analysis of heat clearing and detoxifying drug JC724 on the treatment of colorectal cancer.World journal of gastrointestinal oncology · 2023Article
- Metabolomics coupled with network pharmacology study on the protective effect of Keguan-1 granules in LPS-induced acute lung injury.Pharmaceutical biology · 2022Article
- Impact of e-cigarette aerosol on primary human alveolar epithelial type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Attenuation of Polycyclic Aromatic Hydrocarbon (PAH)-Mediated Pulmonary DNA Adducts and Cytochrome P450 (CYP)1B1 by Dietary Antioxidants, Omega-3 Fatty Acids, in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Molecular mechanisms of pulmonary carcinogenesis by polycyclic aromatic hydrocarbons (PAHs): Implications for human lung cancer.Seminars in cancer biology · 2021Review
- Biological roles of cytochrome P450 1A1, 1A2, and 1B1 enzymes.Archives of pharmacal research · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In 2019, lung cancer was estimated to be the leading cause of cancer deaths in humans. Polycyclic aromatic hydrocarbons (PAHs) are known to increase the risk of lung cancer. PAHs are metabolized by the cytochrome P450 (CYP)1A subfamily, comprised of the CYP1A1 and 1A2 monooxygenases. These enzymes bioactivate PAHs into reactive metabolites that induce mutagenic DNA adducts, which can lead to cancer. Past studies have investigated the role of CYP1A1 in PAH bioactivation; however, the individual roles of each CYP1A enzyme are still unknown. In this investigation, we tested the hypothesis that mice lacking the genes for Cyp1a1 or Cyp1a2 will display altered susceptibilities to PAH-induced pulmonary carcinogenesis. Wild-type, Cyp1a1-null (Cyp1a1-/-), and Cyp1a2-null (Cyp1a2-/-) male and female mice were treated with 3-methylcholanthrene for cancer initiation and tumor formation studies. In wild-type mice, CYP1A1 and 1A2 expression was induced by 3-methylcholanthrene. Cyp1a1-/- and Cyp1a2-/- mice treated with PAHs displayed a compensatory pattern, where knocking out 1 Cyp1a gene led to increased expression of the other. Cyp1a1-/- mice were resistant to DNA adduct and tumor formation, whereas Cyp1a2-/- mice displayed increased levels of both. UALCAN analysis revealed that lung adenocarcinoma patients with high levels of CYP1A2 expression survive significantly better than patients with low/medium expression. In conclusion, Cyp1a1-/- mice were less susceptible to PAH-induced pulmonary carcinogenesis, whereas Cyp1a2-/- mice were more susceptible. In addition, high CYP1A2 expression was found to be protective for lung adenocarcinoma patients. These results support the need to develop novel CYP1A1 inhibitors to mitigate human lung cancer.
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