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Trancriptomic profiling of hepatocytes and mesenchymal cells of rats treated with nongenotoxic carcinogens for up to 2 weeks

ABSTRACT: Conventional notion regards the action of non-genotoxic carcinogens (NGC) an autonomous process largely confined to parenchymal cells. Here we aim to elucidate the role of the hepatic mesenchyme for the action of two prototypical NGC, phenobarbital (PB), an anti-epileptic drug, and cyproterone acetate (CPA) a gestagen used in contraceptive pills.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE68120 | GEO | 2017/07/12

SECONDARY ACCESSION(S): PRJNA281875

REPOSITORIES: GEO

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Trancriptomic profiling of hepatocytes and mesenchymal cells of mice treated with phenobarbital for 2 weeks

Project description:Conventional notion regards the action of non-genotoxic carcinogens (NGC) an autonomous process largely confined to parenchymal cells. Here we aim to elucidate the role of the hepatic mesenchyme for the action of a prototypical NGC, phenobarbital (PB), an anti-epileptic drug.

2017-07-12 | GSE68111 | GEO

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (miRNA)

Project description:In this study we performed microarray-based molecular profiling of liver samples from Wistar rats exposed to genotoxic carcinogens (GC), nongenotoxic carcinogens (NGC) or non-hepatocarcinogens (NC) for up to 14 days. In contrast to previous toxicogenomics studies aimed at the inference of molecular signatures for assessing the potential and mode of compound carcinogenicity, we considered multi-level omics data. Besides evaluating the predictive power of signatures observed on individual biological levels, such as mRNA, miRNA and protein expression, we also introduced novel feature representations which capture putative molecular interactions or pathway alterations by integrating expression profiles across platforms interrogating different biological levels. Male Wistar rats were treated by oral gavage with the eight nongenotoxic hepatocarcinogens Phenobarbital sodium (PB), Piperonylbutoxide (PBO), Dehydroepiandrosterone (DHEA), Acetamide (AA), Methapyrilene HCl (MPy), Methylcarbamate (Mcarb), Diethylstilbestrol (DES) and Ethionine (ETH), the two genotoxic carcinogens C.I Direct Black (CIDB) and dimethylnitrosamine (DMN), the two non-hepatocarcinogens Cefuroxime (CFX) and Nifedipine (Nif), and the three compounds with undefined carcinogenic class Cyproterone acetate (CPA), Thioacetamid (TAA) and Wy-14643 (Wy). Depending on the administered compound, livers were taken after 3, 7, or 14 days for histopathological evaluation. From the five animals per treatment group three animals were selected based on the histopathological findings and subjected to molecular profiling using Affymetrix RG-230A arrays (mRNA expression), Agilent G4473A arrays (miRNA expression) and Zeptosens ZeptoMARK reverse arrays (protein expression).

2014-08-18 | E-GEOD-53083 | biostudies-arrayexpress

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (mRNA)

2014-08-18 | E-GEOD-53082 | biostudies-arrayexpress

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (protein)

2014-08-18 | E-GEOD-53084 | biostudies-arrayexpress

Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]

2013-03-25 | GSE45465 | GEO

Effect of treatment for three months with chemical carcinogen and non-carcinogens on liver miRNAome

2013-07-03 | GSE48492 | GEO

Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]

Project description:Dynamic changes in the mouse liver DNA methylome associated with short (1 day) and prolonged (7, 28 and 91 days) exposure to the rodent liver non-genotoxic carcinogen (NGC), phenobarbital (PB). Full expression dataset (all time points: 1, 7, 28, 91 days) Replicated control vs. pb treated study

2013-03-25 | E-GEOD-45465 | biostudies-arrayexpress

Evidence that the capacity of nongenotoxic carcinogens to induce oxidative stress is subject to marked variability.

Project description:Many drugs and environmental chemicals which are not directly mutagenic have the capacity to increase the incidence of tumors in the liver and other tissues. For this reason, such compounds are known as nongenotoxic carcinogens. The mechanisms underlying their effects remain unclear; however, their capacity to induce oxidative stress is considered to be a critical step in the carcinogenic process, although the evidence that this is actually the case remains equivocal and sparse. We have exploited a novel heme oxygenase-1 reporter mouse to evaluate the capacity of nongenotoxic carcinogens with different mechanisms of action to induce oxidative stress in the liver in vivo. When these compounds were administered at doses reported to cause liver tumors, marked differences in activation of the reporter were observed. 1,4-Dichlorobenzene and nafenopin were strong inducers of oxidative stress, whereas phenobarbital, piperonyl butoxide, cyproterone acetate, and WY14,643 were, at best, only very weak inducers. In the case of phenobarbital and thioacetamide, the number of LacZ-positive hepatocytes increased with time, and for the latter also with dose. The data obtained demonstrate that although some nongenotoxic carcinogens can induce oxidative stress, it is not a dominant feature of the response to these compounds. Therefore in contrast to the current models, these data suggest that oxidative stress is not a key determinant in the mechanism of nongenotoxic carcinogenesis but may contribute to the effects in a compound-specific manner.

| S-EPMC4833039 | biostudies-literature

Effect of treatment for three months with chemical carcinogen and non-carcinogens on liver miRNAome

Project description:Here, we examined the liver microRNA profile of male Fischer rats exposed through their diet to genotoxic (2-acetylaminofluorene) and epigenetic (phenobarbital, diethylhexylphthalate, methapyrilene HCL, monuron, and chlorendic acid) chemical hepatocarcinogens, as well as to non-hepatocarcinogenic treatments (benzophenone, and diethylthiourea) for three months. The aim of the study was to investigate how liver miRNA profiles relate to mode of action and carcinogenic potential of chemicals. In total miRNA profiles from 38 liver samples were examined. These included 3-5 samples for animal fed control diets or diet supplemented with designated chemicals. For each chemical a carcinogenic or a maximum tolerated dose was chosen based on published literature. The treatments were Diethylthiourea (DETU) 2500 ppm; Benzophenone (BP) 1250 ppm ; Monuron (MON) 1500 ppm ; Diethylhexylphthalate (DEHP) 12000 ppm ; Phenobarbital (PB) 1000 ppm; Chlorendic acid (CA) 1250 ppm; Methapyrilene HCl (MP) 250 ppm; 2-Acetyl aminofluorene (2-AAF) 40 ppm.

2013-07-03 | E-GEOD-48492 | biostudies-arrayexpress

FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (mRNA)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate and mifepristone (RU486) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Expression profiling by microarray of LNCaP-1F5 cells treated with vehicle, 100 nM 5a-dihydrotestosterone (DHT), 100 nM dexamethasone (Dex), 1000 nM cyproterone acetate (CPA), 100 nM mifepristone (RU486) and combination of 100 nM DHT,100 nM Dex for 24 hours.

2013-02-05 | E-GEOD-39654 | biostudies-arrayexpress

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