Language

English

Publication Date

11-1-2024

Journal

Environmental and Molecular Mutagenesis

DOI

10.1002/em.22639

PMID

39588573

PMCID

PMC12649781

PubMedCentral® Posted Date

11-27-2025

PubMedCentral® Full Text Version

Author MSS

Abstract

The epigenome is a target for environmental exposures and a potential determinant of inter-individual differences in response. In genetically identical C57Bl/6 mice exposed from gestation to weaning to the endocrine-disrupting chemical (EDC) tributyltin (TBT), hepatic tumor development later in life varied across multiple cohorts over time and depending on sex and diet. In one cohort where approximately half of TBT-exposed male mice developed liver tumors at 10 months (Katz et al. Hepatic tumor formation in adult mice developmentally exposed to organotin, Environmental Health Perspectives, 128 (1), 17010, 2020), transcriptomic (RNA-seq) and epigenomic (ChIP-seq) profiling was performed on blood and liver tissue from mice that developed tumors (i.e., "high-risk") and equivalently exposed mice did not (i.e., "low-risk"). Blood transcriptomic signatures separated TBT-exposed from vehicle controls but did not discriminate between animals that developed tumors versus those that did not. However, uninvolved liver tissue of mice with tumors exhibited transcriptomic and epigenomic signatures distinct from liver tissue of mice without tumors and had many features in common with tumors. These high-risk transcriptomic and epigenomic features were also found in 10/26 TBT-exposed mice at 5 months, indicating that this risk signature preceded tumor development. Thus, while early life exposure to TBT exhibits variable penetrance for hepatic tumor development, indicating TBT exposure is not sufficient for liver tumorigenesis, increased risk for hepatic tumor development is linked to epigenomic and transcriptomic reprogramming of the liver induced by this EDC.

Keywords

Animals, Transcriptome, Mice, Liver Neoplasms, Male, Mice, Inbred C57BL, Female, Trialkyltin Compounds, Endocrine Disruptors, Epigenomics, Liver, Epigenesis, Genetic, endocrine disrupting chemical, tributyltin, liver tumor, epigenome, transcriptome, developmental reprogramming

Published Open-Access

yes

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