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Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67078 | GEO | 2016/05/10

SECONDARY ACCESSION(S): PRJNA278864

REPOSITORIES: GEO

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Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma (MeDIP)

Project description:The study investigated differential gene expression, microRNA expression and DNA methylation changes in a pool of primary human hepatocyte RNA and DNA following 5 days of repetitive exposure to a low or moderate dose of aflatoxin B1 or DMSO. Three biological replicates per compound/solvent. In total 9 arrays.

2016-05-10 | GSE67005 | GEO

Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma (miRNA)

2016-05-10 | GSE67003 | GEO

Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma (Affymetrix)

Project description:The study investigated differential gene expression, microRNA expression and DNA methylation changes in a pool of primary human hepatocyte RNA and DNA following 5 days of repetitive exposure to a low (LD) or moderate (MD) dose of aflatoxin B1 or DMSO. Three biological replicates per compound/solvent.

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Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma

Project description:Aflatoxin B1 exposure induces epigenetic mechanisms in primary human hepatocytes revealing novel biological processes associated with hepatocellular carcinoma

| PRJNA278864 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-05-10 | GSE71549 | 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

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

2016-05-10 | GSE71545 | GEO

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

2016-05-10 | GSE71548 | GEO

Aflatoxin B1 DNA-Adducts in Hepatocellular Carcinoma from a Low Exposure Area.

Project description:Aflatoxin B1 (AFB1) is a class 1 carcinogen with an ascertained role in the development of hepatocellular carcinoma (HCC) in high exposure areas. Instead, this study aimed to assay whether chronic/intermittent, low-dose AFB1 consumption might occur in low-exposure geographical areas, ultimately accumulating in the liver and possibly contributing to liver cancer. AFB1-DNA adducts were assayed by immunostaining in liver tissues from three Italian series of twenty cirrhosis without HCC, 131 HCC, and 45 cholangiocarcinoma, and in an AFB1-induced HCC rat model. CD68, TP53 immunostaining, and TP53 RFLP analysis of R249S transversion were used to characterize cell populations displaying AFB1-DNA adducts. Twenty-five HCCs displayed AFB1-adducts both in neoplastic hepatocytes and in cells infiltrating the tumor and non-tumor tissues. Nuclear immunostaining was observed in a few cases, while most cases showed cytoplasmic immunostaining, especially in CD68-positive tumor-infiltrating cells, suggestive for phagocytosis of dead hepatocytes. Similar patterns were observed in AFB1-induced rat HCC, though with higher intensity. Cholangiocarcinoma and cirrhosis without HCC did not displayAFB1-adducts, except for one case. Despite not providing a causal relationship with HCC, these findings still suggest paying attention to detection and control measures for aflatoxins to ensure food safety in low exposure areas.

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Aflatoxin B1 invokes apoptosis via death receptor pathway in hepatocytes.

Project description:The fungal metabolites produced by Aspergillus flavus and Aspergillus parasiticus cause detrimental health effects on humans and animals. Particularly aflatoxin B1 (AFB1) is the most studied and a well-known global carcinogen, producing hepatotoxic, genotoxic and immunotoxic effects in multiple species. AFB1 is shown to provoke liver dysfunctioning by causing hepatocytes apoptosis and disturbing cellular enzymatic activities. In liver, AFB1 causes apoptosis via extrinsic mechanism because of high expression of death receptor pathway. The detailed mechanism of AFB1 induced hepatocytes apoptosis, via death receptor pathway still remains elusive. So the present study was conducted to explore apoptotic mechanism initiated by death receptors and associated genes in aflatoxin B1 induced liver apoptosis in chickens fed with AFB1 for 3 weeks. Results from the present study displayed histopathological and ultrastructural changes in liver such as hydropic degeneration, fatty vacuolar degeneration and proliferation of bile duct in hepatocytes in AFB1 group, along with imbalance between reactive oxygen species (ROS) and antioxidant defense system upon AFB1 ingestion. Moreover, AFB1 intoxicated chickens showed upregulation of death receptors FAS, TNFR1 and associated genes and downregulation of inhibitory apoptotic proteins XIAP and BCL-2. The results obtained from this novel and comprehensive study including histopathological, ultrastructural, flow cytometrical and death receptor pathway gene expression profiles, will facilitate better understanding of mechanisms and involvement of death receptor pathway in hepatocytes apoptosis induced by AFB1 and ultimately may be helpful in bringing down the toxigenic potential of AFB1.

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