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Gene expression in liver of wild-type and Dicer1-KO mice treated with genotoxic carcinogen N-ethyl-N-nitrosourea

ABSTRACT: To explore the possible changes of gene expression induced by a carcinogen, we treated wild-type and Dicer1-KO mice with one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU), a model genotoxic carcinogen, and vehicle control. The gene expression profiles were assessed in the mouse livers in wild-type and Dicer1-KO mice design. Total RNA were isolated from the livers at days 15 after the treatment and their expression was determined using Gene Array.

ORGANISM(S): Mus musculus

PROVIDER: GSE36307 | GEO | 2012/03/06

SECONDARY ACCESSION(S): PRJNA153055

REPOSITORIES: GEO

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Gene expression in liver of wild-type and Dicer1-KO mice treated with genotoxic carcinogen N-ethyl-N-nitrosourea

Project description:To explore the possible changes of gene expression induced by a carcinogen, we treated wild-type and Dicer1-KO mice with one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU), a model genotoxic carcinogen, and vehicle control. The gene expression profiles were assessed in the mouse livers in wild-type and Dicer1-KO mice design. Total RNA were isolated from the livers at days 15 after the treatment and their expression was determined using Gene Array. Gene expression in treated wild-type and Dicer1-KO mice was measured at 15 days after exposure to one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU). Each treatment duplex ,Drug-ko-a,Drug-ko-b,Drug-wt-a,Drug-wt-b,Control-ko-a,Control-ko-b,Control-wt-a,Control-wt-b.

2012-03-06 | E-GEOD-36307 | biostudies-arrayexpress

Genomic analysis of microRNA time-course expression in liver of mice treated with genotoxic carcinogen N-ethyl-N-nitrosourea

Project description:Dysregulated expression of microRNA (miRNA) has been extensively detected in human cancer tissues and has shown promise in defining tumor status. It, however, is little known whether and when expression of miRNAs can be changed in normal tissues after carcinogen exposure. To explore possible time-course changes of miRNA expression induced by carcinogens, we treated mice with one dose of 120 mg/kg body weight model genotoxic carcinogen N-ethyl-N-nitrosourea (ENU) and vehicle control. The miRNA expression profiles were determined in the mouse livers in a time-course manner. MiRNAs were isolated from the livers of ENU-treated and control mice at days 1, 3, 7, 15, 30 and 120 after the treatment. The miRNA expressions were determined using RT2-mouse miRNA PCR Array. Principal component analysis of the gene expression profiles showed that miRNA expression at post-treatment days 7 and 15 were different from those at the other time points and the controls. The numbers of the dysregulated miRNAs changed with time, being 3, 5, 14, 32, 5 and 5 at post-treatment days 1, 3, 7, 15, 30 and 120, respectively. Functional analysis of the differentially expressed miRNA at post-treatment days 7 and 15 indicated that the major functions of these ENU-induced dysregulated miRNAs were mainly associated with DNA repair and tumorigenesis, suggesting the microRNA expression is related to genotoxicity of ENU. These results propose that one to two weeks after ENU exposure is the best time for miRNA expression sampling; and that a large number of miRNAs whose expression is dysregulated after carcinogen exposure could be an indicator for carcinogenic damage. Series type: Non-coding RNA profiling by RT-PCR

2010-11-04 | GSE20248 | GEO

Mus musculus

Project description:Gene expression in liver of wild-type and Dicer1-KO mice treated with genotoxic carcinogen N-ethyl-N-nitrosourea

| PRJNA153055 | ENA

Negative selection allows human primary fibroblasts to tolerate high somatic mutation loads induced by N-ethyl-N-nitrosourea

Project description:Single-cell sequencing has shown that thousands of mutations accumulate with age in most human tissues. While there is ample evidence that some mutations can clonally amplify and lead to disease, the total burden of mutations a cell tolerates without functional decline remains unknown. Here we addressed this question by exposing human primary fibroblasts to multiple, low doses of N-ethyl-N-nitrosourea (ENU) and analyzed somatic mutation burden using single-cell whole genome sequencing. The results indicate that individual cells can sustain ~60,000 single-nucleotide variants (SNVs) with only a slight adverse effect on growth rate. We provide evidence that such high levels of mutations are only tolerated through negative selection against variants in gene coding regions, and in sequences associated with genetic pathways for maintaining basic cellular function and growth. Since most tissues in adults are non-dividing, these results suggest that somatic mutations in the absence of negative selection may have functionally adverse effects.

2024-07-22 | GSE271867 | GEO

Microarray analysis of Caenorhabditis elegans exposed to three hydrophilic genotoxicants in water in duplicate

Project description:In this study, we exposed Caenorhabditis elegans wild types N2 to two concentrations of the model genotoxicants formaldehyde (HCHO), N-ethyl-N-nitrosourea (ENU), and methyl methanesulfonate (MMS).We performed a concentration-response test to determine the non-toxic concentration range for studying the transcriptional effects of compounds. In microarray experiments, we studied two concentrations (1 mM and 5 mM) for each compound and a control of M9 medium. Age synchronized worms at developmental L4 larval stage were exposed to treatment for two hours. After flash freezing the samples, RNA was isolated, labeled and hybridized on oligo microarray (Agilent) slides.

2021-04-23 | E-MTAB-10264 | biostudies-arrayexpress

Microarray analysis of Caenorhabditis elegans exposed to three hydrophilic genotoxicants in water

Project description:In this study, we exposed Caenorhabditis elegans wild types N2 to two concentrations of the model genotoxicants formaldehyde (HCHO), N-ethyl-N-nitrosourea (ENU), and methyl methanesulfonate (MMS).We performed a concentration-response test to determine the non-toxic concentration range for studying the transcriptional effects of compounds. In microarray experiments, we studied two concentrations (1 mM and 5 mM) for each compound and a control of M9 medium. Age synchronized worms at developmental L4 larval stage were exposed to treatment for four hours. After flash freezing the samples, RNA was isolated, labeled and hybridized on oligo microarray (Agilent) slides.

2021-04-23 | E-MTAB-10265 | biostudies-arrayexpress

RNA-seq for MP, AML and MEFs from mice that carry a "knock-in" allele of the mutant splicing factor, U2af1(S34F), with or without homozygous deletion of the transcription factor, Runx1

Project description:We have generated mice that carry Cre-dependent "knock-in" alleles (MGS34F and IES34F) of U2af1(S34F), a mutation commonly encountered in human myelodysplastic syndromes and acute myeloid leukemia (AML). MEFs were generated from the progenies of these mice with those carrying a UBC-CreERT2 transgene, and were treated with 4-Hydroxytamoxifen (4OHT) to induce Cre-mediated recombination and subsequent U2af1(S34F) expression. Mice carrying the MGS34F allele were further crossed with those carrying a floxed Runx1 allele and Mx1-Cre. U2af1(S34F) expression and Runx1 deletion caused changes in gene expression and RNA splicing. Mice with a conditional "knock-in" U2af1(S34F) allele and conditional "knockout" alleles of Runx1 were mutagenized with low-dose N-Ethyl-N-Nitrosourea (ENU). Within 1.5 year, one of fourteen ENU-treated mice with U2af1(S34F) and Runx1 deletion developed AML, as did recipients of allografted splenic cells from two other such mice, but AML did not arise from cells with other genotypes or mice without ENU treatment.

2018-07-26 | GSE112174 | GEO

Proximity Proteomics Revealed Dicer1 and Transporters as Client Proteins of Aha1

Project description:Co-chaperone Aha1 activates HSP90 ATPase to promote the folding of client proteins. However, the client proteins of Aha1 are largely unknown. By employing ascorbate peroxidase (APEX) based proximity labeling, we identified 32 proximity proteins of HSP90 that are modulated by genetic depletion of Aha1. Among them, Dicer1 is one of the top-ranked proteins, which were further confirmed by streptavidin pull-down followed by Western blot analysis, demonstrating the reliability of the approach. Flag pull-down result showed interactions between endogenous HSP90 and Dicer1 and Aha1. The Dicer1 level is regulated synergistically by Aha1 and HSP90. Maturation-dependent interaction results showed a preferential binding of Aha1 and HSP90 to nascently translated Dicer1. Reconstitution of Aha1-depleted cells with WT Aha1 restored Dicer1 level, while the HSP90-binding-defective E67K mutant exhibited partial restoration. Moreover, knockdown of Aha1 and inhibition of HSP90 can diminish the levels of mature miRNA, let-7b and mir-30a. Overall, our study uncovers, for the first time, Dicer1 and transporter proteins as clients of Aha1 and HSP90.

2022-11-19 | PXD028980 | Pride

Genomic characterization of DICER1-associated neoplasms uncovers novel molecular classes

Project description:DNA methylation data of a novel group of mesenchymal tumors with DICER1 alteration which includes two novel classes designated “low-grade mesenchymal tumor with DICER1 alteration” (LGMT DICER1) and “high-grade sarcoma with DICER1 alteration” (HGS DICER1), as well as the recently described class of primary intracranial sarcoma, DICER1-mutant (PIS DICER1)

2023-02-08 | GSE214568 | GEO

Effects of ethyl carbamate exposure on C. elegans transcriptome

Project description:Ethyl carbamate is a common food contaminant prevalent in fermented food with probable carcinogenic effects in animals. To date, other toxicological properties of ethyl carbamate are not well characterized. Using the genetic model Caenorhabditis elegans, we found that chronic exposure to ethyl carbamate during larval development inhibits growth while exposure at adulthood inhibits reproduction, shortens lifespan, and promotes degeneration of dopaminergic neurons. Through whole-transcriptome RNA-sequencing, we found that ethyl carbamate invokes a widespread transcriptomic response inducing the differential expression of > 4,000 genes by at least 2-fold. Functional analysis of RNA-sequencing data revealed that genes up-regulated enrich to various neuron regulatory processes and xenobiotic defense. Gene expression analysis confirms that various genes functioning within phase 1 and 2 detoxification responses along with ABC transporters are highly up-regulated in response to ethyl carbamate exposure, suggesting the induction of oxidative stress. Overall, these findings demonstrates new toxicological properties of chronic ethyl carbamate exposure and provide new insights into the effects in has on transcriptome regulation in the C. elegans model.

2022-04-13 | GSE190099 | GEO

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