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• W2020119521 abstract "A single human cell contains more than 5.0 × 105 copies of long interspersed element-1 (L1), 80–100 of which are competent for retrotransposition (L1-RTP). Recent observations have revealed the presence of de novo L1 insertions in various tumors, but little is known about its mechanism. Here, we found that 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline (MeIQx), food-borne carcinogens that are present in broiled meats, induced L1-RTP. This induction was dependent on a cellular cascade comprising the aryl hydrocarbon receptor (AhR), a mitogen-activated protein kinase, and CCAAT/enhancer-binding protein β. Notably, these compounds exhibited differential induction of L1-RTP. MeIQx-induced L1-RTP was dependent on AhR nuclear translocator 1 (ARNT1), a counterpart of AhR required for gene expression in response to environmental pollutants. By contrast, PhIP-induced L1-RTP did not require ARNT1 but was dependent on estrogen receptor α (ERα) and AhR repressor. In vivo studies using transgenic mice harboring the human L1 gene indicated that PhIP-induced L1-RTP was reproducibly detected in the mammary gland, which is a target organ of PhIP-induced carcinoma. Moreover, picomolar levels of each compound induced L1-RTP, which is comparable to the PhIP concentration detected in human breast milk. Data suggest that somatic cells possess machineries that induce L1-RTP in response to the carcinogenic compounds. Together with data showing that micromolar levels of heterocyclic amines (HCAs) were non-genotoxic, our observations indicate that L1-RTP by environmental compounds is a novel type of genomic instability, further suggesting that analysis of L1-RTP by HCAs is a novel approach to clarification of modes of carcinogenesis." @default.
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• W2020119521 date "2012-12-03" @default.
• W2020119521 modified "2023-10-17" @default.
• W2020119521 title "Long interspersed element-1 is differentially regulated by food-borne carcinogens via the aryl hydrocarbon receptor" @default.
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• W2020119521 doi "https://doi.org/10.1038/onc.2012.516" @default.
• W2020119521 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3795476" @default.
• W2020119521 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23208499" @default.
• W2020119521 hasPublicationYear "2012" @default.
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