Transcriptome analysis of Caco-2 Cells upon deoxynivalenol and its acetylated exposure
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ABSTRACT:
PROVIDER: PRJNA690062 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13367368_1.fastq.gz | Fastqsanger.gz | |||
| SRR13367368_2.fastq.gz | Fastqsanger.gz | |||
| SRR13367369_1.fastq.gz | Fastqsanger.gz | |||
| SRR13367369_2.fastq.gz | Fastqsanger.gz | |||
| SRR13367370_1.fastq.gz | Fastqsanger.gz |
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Project description:Deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-ADON) and 15-acetyldeoxynivalenol (15-ADON) are type B trichothecenes and are major pollutants in food and feed products. Although the toxicity of DON has been well documented, the information of toxicity of its acetylated derivative remains incomplete. To acquire more detailed insight in 3-ADON and 15-ADON, Caco-2 cells under 0.5 µM DON, 3-ADON and 15-ADON treatment for 24 h were subjected to RNA-seq analysis. In the present study, 2656, 3132 and 2425 differentially expressed genes (DEGs) were selected respectively and were enriched utilizing KEGG and GO database. The upregulation of ataxia-telangiectasia mutated kinase (ATM), WEE1 homolog 2 (WEE2) and downregulation of proliferating cell nuclear antigen (PCNA), minichromosome maintenance (MCMs), cyclin dependent kinase (CDKs), E2Fs indicate that the three toxins induced DNA damage, inhibition of DNA replication and cell cycle arrest in Caco-2 cells. Apart from these, the upregulation of sestrin (SENEs) and NEIL1 implied that the reason of DNA damage may attribute to oxidative stress. Our study provides an insight in the toxic mechanism of 3-ADON and 15-ADON.
2021-01-07 | GSE164334 | GEO
Project description:To screen cellular effects on Caco-2 cells by deoxynivalenol (DON) and 15-acetyldeoxynivalenol (15ADON), toxin-treated Caco-2 cells were analyzed by DNA microarray. Exposure to either toxin induced up- or downregulation of genes in Caco-2 cells. Upregulation of 1290 and 3238 genes was observed for the DON- and 15ADON-treated groups, respectively, after a 60-min incubation period. This represented a greater than 1.5-fold change relative to the 0-min exposure (control) group. Five hundred and sixty-one genes showed a 1.5-fold upregulation in the both the DON- and 15ADON-treated groups. Similarly, 13 genes and 105 genes were upregulated with a log2 ratio > 2 (4-fold change) in the DON- and 15ADON-treated groups, respectively. The most remarkable gene upregulation corresponded to the inflammatory chemokine, IL-8, which showed a greater than 4-fold upregulation in response to both treatments. Deoxynivalenol and 15-acetyldeoxynivalenol at concentrations of 1 ug/mL were added separately to the AP chamber, and cells were harvested with 0.5% trypsin-EDTA after incubation for 0, 5, 30, and 60 min. Toxin-treated Caco-2 cells were analyzed by DNA microarray to screen for changes in gene expression in response to deoxynivalenol or 15-acetyldeoxynivalenol.
2013-02-27 | E-GEOD-44716 | biostudies-arrayexpress
Project description:Deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-ADON) and 15-acetyldeoxynivalenol (15-ADON) are type B trichothecenes; one of the major pollutants in food and feed products. Although the toxicity of DON has been well documented, information on the toxicity of its acetylated derivative remains incomplete. To acquire more detailed insight into 3-ADON and 15-ADON, Caco-2 cells under 0.5 µM DON, 3-ADON and 15-ADON treatment for 24 h were subjected to RNA-seq analysis. In the present study, 2656, 3132 and 2425 differentially expressed genes (DEGs) were selected, respectively, and were enriched utilizing the Kyoto Encyclopedia of Genes and Genomes (KEGG) and the Gene Ontology (GO) database. The upregulation of ataxia-telangiectasia mutated kinase (ATM), WEE1 homolog 2 (WEE2) and downregulation of proliferating cell nuclear antigen (PCNA), minichromosome maintenance (MCMs), cyclin dependent kinase (CDKs), and E2Fs indicate that the three toxins induced DNA damage, inhibition of DNA replication and cell cycle arrest in Caco-2 cells. Additionally, the upregulation of sestrin (SENEs) and NEIL1 implied that the reason for DNA damage may be attributable to oxidative stress. Our study provides insight into the toxic mechanism of 3-ADON and 15-ADON.
| S-EPMC7927021 | biostudies-literature
Project description:To screen cellular effects on Caco-2 cells by deoxynivalenol (DON) and 15-acetyldeoxynivalenol (15ADON), toxin-treated Caco-2 cells were analyzed by DNA microarray. Exposure to either toxin induced up- or downregulation of genes in Caco-2 cells. Upregulation of 1290 and 3238 genes was observed for the DON- and 15ADON-treated groups, respectively, after a 60-min incubation period. This represented a greater than 1.5-fold change relative to the 0-min exposure (control) group. Five hundred and sixty-one genes showed a 1.5-fold upregulation in the both the DON- and 15ADON-treated groups. Similarly, 13 genes and 105 genes were upregulated with a log2 ratio > 2 (4-fold change) in the DON- and 15ADON-treated groups, respectively. The most remarkable gene upregulation corresponded to the inflammatory chemokine, IL-8, which showed a greater than 4-fold upregulation in response to both treatments.
2013-02-27 | GSE44716 | GEO
Project description:It has been proposed that chronic exposure to deoxynivalenol modulates hepatic gene expression and that sensivity to xenobiotics like deoxynivalenol is modulated by inflammation. We used microarrays to evaluate whether chronic deoxynivalenol exposure influences the hepatic gene expression of Sus scrofa in vivo and whether interaction between chronic deoxynivalenol exposure and systemic inflammation occur.
2021-07-19 | GSE171991 | GEO
Project description:N-nitroso compounds (NOC) may be implicated in human colon carcinogenesis, but the toxicological mechanisms involved have not been elucidated. Since it was previously demonstrated that nitrosamines and nitrosamides, representing two classes of NOC, induce distinct gene expression effects in colon cells that are particularly related to oxidative stress, we hypothesized that different radical mechanisms are involved. Using ESR spectroscopy, we investigated radical generating properties of genotoxic NOC concentrations in human colon adenocarcinoma cells (Caco-2). Cells were exposed to nitrosamides (N-methyl-N'-nitro-N-nitrosoguanidine, N-methyl-N-nitrosurea) or nitrosamines (N-nitrosodiethylamine, N-nitrosodimethylamine, N-nitrosopiperidine, N-nitrosopyrrolidine). Nitrosamines caused formation of reactive oxygen species (ROS) and carbon centered radicals which was further stimulated in presence of Caco-2 cells. N-methyl-N-nitrosurea exposure resulted in a small ROS signal, and formation of nitrogen centered radicals (NCR), also stimulated by Caco-2 cells. N-methyl-N'-nitro-N-nitrosoguanidine did not cause radical formation at genotoxic concentrations, but at increased exposure levels, both ROS and NCR formation was observed. By associating gene expression patterns with ROS formation, several cellular processes responding to nitrosamine exposure were identified, including apoptosis, cell cycle blockage, DNA repair and oxidative stress. These findings suggest that following NOC exposure in Caco-2 cells, ROS formation plays an important role in deregulation of gene expression patterns which may be relevant for the process of chemical carcinogenesis in the human colon, in addition to the role of DNA alkylation. Keywords: Nitrosamines, nitrosamides, N-nitroso compounds, free radicals, toxicogenomics, colon carcinogenesis The study investigated differential gene expression in Caco-2 cell line mRNA following 1, 6 or 24 hours of exposure to six different N-nitroso compounds. Two biological replicates per sample compound. One compound per array, hybridized against vehicle control. Dye-swap between biological replicates.
2010-05-28 | E-GEOD-20993 | biostudies-arrayexpress
Project description:N-nitroso compounds (NOC) may be implicated in human colon carcinogenesis, but the toxicological mechanisms involved have not been elucidated. Since it was previously demonstrated that nitrosamines and nitrosamides, representing two classes of NOC, induce distinct gene expression effects in colon cells that are particularly related to oxidative stress, we hypothesized that different radical mechanisms are involved. Using ESR spectroscopy, we investigated radical generating properties of genotoxic NOC concentrations in human colon adenocarcinoma cells (Caco-2). Cells were exposed to nitrosamides (N-methyl-N'-nitro-N-nitrosoguanidine, N-methyl-N-nitrosurea) or nitrosamines (N-nitrosodiethylamine, N-nitrosodimethylamine, N-nitrosopiperidine, N-nitrosopyrrolidine). Nitrosamines caused formation of reactive oxygen species (ROS) and carbon centered radicals which was further stimulated in presence of Caco-2 cells. N-methyl-N-nitrosurea exposure resulted in a small ROS signal, and formation of nitrogen centered radicals (NCR), also stimulated by Caco-2 cells. N-methyl-N'-nitro-N-nitrosoguanidine did not cause radical formation at genotoxic concentrations, but at increased exposure levels, both ROS and NCR formation was observed. By associating gene expression patterns with ROS formation, several cellular processes responding to nitrosamine exposure were identified, including apoptosis, cell cycle blockage, DNA repair and oxidative stress. These findings suggest that following NOC exposure in Caco-2 cells, ROS formation plays an important role in deregulation of gene expression patterns which may be relevant for the process of chemical carcinogenesis in the human colon, in addition to the role of DNA alkylation. Keywords: Nitrosamines, nitrosamides, N-nitroso compounds, free radicals, toxicogenomics, colon carcinogenesis
2010-04-29 | GSE20993 | GEO
Project description:This project has two goals. Firstly, to compare the gene expression profiles of Caco cells following exposure to Verocytotoxigenic E. coli0157:H7 (VTEC) isolates from food animals (bovine, ovine, porcine) and human in an effort to assess the invasive and toxigenic potential of isolates of different origin. All sources contain the common virulence and type 3 secretory system genes. Secondly, to compare the gene expression profiles of Caco-2 cells following exposure to VTEC isolates that contain (positive) or do not contain (negative) the genes of the type 3 secretory system (TTSS).
2017-09-04 | GSE80491 | GEO
Project description:Deoxynivalenol (DON) is an important Fusarium toxin of concern for food safety. The inhalation of powder contaminated with deoxynivalenol is possible and may cause lung toxicity. In this study, we investigated the gene expression profile of A549 cells treated with 0.2 microg/mL deoxynivalenol by microarray analysis. In total, 16 genes and 5 noncoding RNAs were significantly affected by deoxynivalenol treatment.
2016-02-29 | GSE60928 | GEO
Project description:Deoxynivalenol (DON) is an important Fusarium toxin of concern for food safety. The inhalation of powder contaminated with deoxynivalenol is possible and may cause lung toxicity. In this study, we investigated the gene expression profile of A549 cells treated with 0.2 microg/mL deoxynivalenol by microarray analysis. In total, 16 genes and 5 noncoding RNAs were significantly affected by deoxynivalenol treatment. 4 samples; 2 samples from nontreated cells and other 2 samples from 0.2 microg/mL DON-treated cells for 24 hours
2016-02-29 | E-GEOD-60928 | biostudies-arrayexpress