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Combining multiple omics with molecular dynamics reveals SCP2-mediated intestinal toxicity of Aflatoxin B1

ABSTRACT: This study aims to explore the mechanism of AFB1-induced toxicity damage in SW480 cells through the epigenetics, proteomics, and metabolomics, and experimental verification.

ORGANISM(S): Homo sapiens

PROVIDER: GSE269450 | GEO | 2026/06/08

REPOSITORIES: GEO

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Comparative toxicity of Aflatoxin B1, Patulin and their biosynthetic precursors: A human intestinal microarray analysis

Project description:Patulin (PAT) and Aflatoxin B1 (AFB1) are frequent mycotoxins contaminating food and feed which demonstrate multiple toxic effects. These mycotoxins represent final product in cascades of enzymatic reactions. In order to limit the risk generated by food contamination, approaches aiming to block the biosynthesis pathway of these mycotoxins can be considered, provided that their precursors are devoid of toxicity. The aim of this study was to compare the toxicity of two precursor compounds (Versicolorin A (VERA), sterigmatocystin (STG)) to AFB1 and the precursor compound (ascladiol) to PAT. Human intestinal Caco-2 cells were exposed to 1 µM AFB1, VERA, STG or 3 µM PAT or ascladiol for 24 hours and transcription analysis was performed using an “Agilent Sureprint 63 Human GE 8x60k microarray.

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Involvement of Wnt/β-catenin Signaling Pathway in Curdione-Induced Reproductive Toxicity Revealed by Multiomics Profiling in HTR-8/SVneo Cells

Project description:This study aims to explore the mechanism of curdione-induced toxicity damage in HTR-8/SVneo cells through the epigenetics, proteomics, and metabolomics, and experimental verification.

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Project description:Aflatoxin B1 (AFB1) is a mycotoxin produced by Aspergillus flavus and A. parasiticus. AFB1 targeted gene expression profiles were determined in human primary trophoblast cells, isolated from full term placentae after delivery, and exposed to 1 µM AFB1 for 72 hours. Gene expression profiling conducted with human HT-12 expression beadchips

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Project description:Chronic exposure to aflatoxin B1 (AFB1) has, in certain regions in the world, been strongly associated with the development of hepatocellular carcinoma (HCC). AFB1 is a very potent hepatotoxic and carcinogenic mycotoxin which is frequently reported as a food contaminant. Epigenetic modifications provoked by environmental exposures, such as AFB1, may create a so called persistent "epigenetic memory" or "footprint". Deregulation of epigenetic mechanisms has actually been reported in HCC patients following AFB1 exposure; however no attempts have yet been made to investigate early effects on the epigenome level which may be persistent on longer term thereby possibly initiating carcinogenic events. In this study, we aim to identify methyl DNA-mRNA-interactions representative for a persistent epigenetic "footprint" associated with the early onset of AFB1-induced HCC. For this, primary human hepatocytes were exposed to 0.3 µM of AFB1 for 5 days. Persistent epigenetic effects were m easured 3 days after terminating the carcinogenic treatment. Whole genome DNA methylation changes and whole genome transcriptomic analysis were analyzed applying microarray technologies, and cross-omics interactions were evaluated. Upon combining transcriptomics data with results on DNA methylation, a range of persistent hyper- and hypomethylated genes was identified which appeared also affected on the transcriptome level. For six of the hypomethylated and upregulated genes, namely TXNRD1, PCNA, CCNK, DIAPH3, RAB27A and HIST1H2BF, a clear role in carcinogenic events could be identified. This study is the first to report on a carcinogen-induced persistent impact on the "epigenetic footprint" in relation with the transcriptome which could be indicative for the early onset of AFB1-related development of HCC.

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