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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [RNA-seq]

ABSTRACT: Explore the potential downstream signaling pathways that resist AFB1 toxicity after knocking out BACH1 by RNA-seq analysis.

ORGANISM(S): Sus scrofa

PROVIDER: GSE199385 | GEO | 2022/03/25

REPOSITORIES: GEO

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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Aflatoxin B1 (AFB1) is amongst the mycotoxins commonly affecting human and animal health, raising global food safety and control concerns. The mechanisms underlying AFB1 toxicity are poorly understood. Moreover, antidotes against AFB1 are lacking. Genome-wide CRISPR/Cas9 knockout screening in porcine kidney cells identified the transcription factor BTB and CNC homolog 1 (BACH1) as a gene required for AFB1 toxicity. The inhibition of BACH1 expression in porcine kidney cells and human hepatoma cells resulted in increased resistance to AFB1. BACH1 depletion attenuates AFB1-induced oxidative damage via the upregulation of antioxidant genes.

2022-03-25 | GSE199384 | GEO

Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage

Project description:Overall data for CRISPR screening + RNA-Seq

2022-03-25 | GSE199386 | GEO

Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage（CRISPR screening）

Project description:Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage（CRISPR screening）

| PRJNA819546 | ENA

Transcriptional Responses in Livers of Adult and Newborn Mice to Aflatoxin B1

Project description:Susceptibility to the hepatocarcinogen Aflatoxin B1 (AFB1) varies among species and with age. Mice are refractory to carcinogenic and toxic effects of AFB1; however, B6C3F1 mice show transient sensitivity if dosed shortly after birth. We compared age-related differences in gene expression and transcriptional responses to AFB1 in livers of newborn (4-day-old) and adult mice. Keywords: Transcriptional response to a carcinogen

2009-01-01 | GSE4740 | GEO

Early target genes of aflatoxin B1 in human hepatic cells

Project description:Comparison of gene expression profiles induced by the mycotoxin, aflatoxin B1 (AFB1), in primary human hepatocytes and HepaRG cells. Initial mechanisms involved in the complex multistep process leading to malignant transformation by chemicals remain largely unknown. We have analysed changes in gene expression profiles in primary human hepatocytes and differentiated human hepatoma HepaRG cells after a 24 h treatment with 0.05 or 0.25µM aflatoxin B1 (AFB1), a potent genotoxic hepatocarcinogen. Three independent biological replicates of HepaRG cell cultures and two pools of three primary human hepatocyte cultures each, were investigated. Cells were treated with 0.05 or 0.25µM AFB1 for 24 h.

2010-12-07 | E-GEOD-25844 | biostudies-arrayexpress

Early target genes of aflatoxin B1 in human hepatic cells

2010-12-07 | GSE25844 | GEO

Aflatoxin B1 attenuates endocrine function, protein synthesis and energy production of human primary trophoblast

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

2020-12-31 | GSE153590 | GEO

Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage

Project description:Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage

| PRJNA819542 | ENA

Effects of aflatoxin B1 on metabolism- and immunity-related gene expression in Hermetia illucens L. (Diptera: Stratiomyidae)

Project description:Contamination of food products with mycotoxins such as aflatoxin B1 (AFB1) poses a severe risk to human health. Larvae of the black soldier fly (BSFL), Hermetia illucens (Diptera: Stratiomyidae), can successfully metabolize AFB1 without any negative consequences on their survival or growth. However, the underlying mechanisms that allow BSFL to metabolize AFB1 are unknown. In this study, five-day-old BSFL were fed with either a control or an AFB1-spiked (20 µg/kg) diet to elucidate the underlying mechanisms. Larval samples were collected at three timepoints (6 h, 24 h, and 72 h) and subjected to RNA-Seq analysis to determine gene expression patterns. Provision of an AFB1-spiked diet resulted in an up-regulation of 357 and a down-regulation of 929 unique genes. Upregulated genes include multiple genes involved in AFB1 metabolism in other (insect) species. Downregulated genes were generally involved in the insects' growth, development, and immunity. BSFL possesses a diverse genetic arsenal that encodes for enzymes capable of metabolizing AFB1 without trade-offs on larval survival.

2024-06-18 | GSE263746 | GEO

Aflatoxin B1 induces persistent epigenomic effects in primary human hepatocytes associated with hepatocellular carcinoma [mRNA]

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.

2016-05-10 | GSE71547 | GEO

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