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Hepatic expression data from 2-stage carcinogenesis study in rats

ABSTRACT: Hepatic gene expression profiles in 2-stage carcinogenesis study were analyzed with comprehensive DNA methylation data. Combined analysis suggested that PTEN signaling and immune response such as antigen presentation was related to one side of early heapatocarcinogenesis. We used microarrays to obtain the global gene expression profile of livers to understand the mechanism of carcinogenesis.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE51797 | GEO | 2016/10/24

SECONDARY ACCESSION(S): PRJNA225035

REPOSITORIES: GEO

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Hepatic expression data from 2-stage carcinogenesis study in rats

Project description:Hepatic gene expression profiles in 2-stage carcinogenesis study were analyzed with comprehensive DNA methylation data. Combined analysis suggested that PTEN signaling and immune response such as antigen presentation was related to one side of early heapatocarcinogenesis. We used microarrays to obtain the global gene expression profile of livers to understand the mechanism of carcinogenesis. Rat livers sampled at the timing of partial hepatectomy and terminal euthanasia were subjected to RN extraction and hybridization on Affymetrix microarrays. We sought to obtain hepatic gene expression data treated with various initiators and their succession. Briefly, each liver at 5w (partial hepatectomized sample) and 10w (terminal sample) from same animal were subjected to microarray analysis. MC (methylcellulose) and water mean vehicle of initiator and promoter, respectively. As an initiator, diethylnitrosamine (DEN), thioacetamide (TAA), methapyrilene (MP) and acetaminophen (APAP) were administered. As a promoter, phenobarbital (PB) was given in drinking water.

2016-10-24 | E-GEOD-51797 | biostudies-arrayexpress

Genome-wide DNA methylation analysis of livers obtained from 2-stage carcinogenesis model in rats

Project description:Identification of epigenetic alterations in the early stage of carcinogenesis promises a great contribution for mechanism analysis and marker exploration for the drug development. For this purpose, we conducted comprehensive analyses for DNA methylation and gene expression in livers obtained from a rat 2-stage carcinogenesis study using nitrosodiethylamine, thioacetamide, methapyrilene and acetaminophen as an initiator and phenobarbital as a promoter. Here, we report the result of MeDIP-seq using methylated DNA enriched by MBD2-protein in rat livers. Comprehensive gene expression analysis was also conducted using same liver samples. The obtained tag sequences were mapped onto rat genome and arbitrary tag count values were calculated and used as each gene DNA methylation state. Using these methylation and gene expression data, pathway analyses for each treatment was performed. The data indicated that livers accompanying preneoplastic legions acquired carcinogenic character of DNA methylation and immune-response related pathways were affected.

2016-12-19 | GSE53518 | GEO

PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

Project description:PTEN, a widely investigated tumor suppressor, has at least two longer translational variants, PTEN and . However, the regulation and precise roles of endogenous PTEN/ in tumorigenesis remain greatly unknown. Here we show that USP9X and FBXW11 selectively regulate the stability of PTEN/ but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTEN/. In contrast to the current paradigm for PTEN as a tumor suppressor, PTEN/ promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTEN/ localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTEN/ but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature. Taken together, our results indicate that PTEN/ are a double-edged sword for carcinogenesis, suggesting that reinterpretation of the importance of PTEN gene in carcinogenesis is warranted.

2019-11-14 | PXD013196 | Pride

Epigenetic reprogramming in hepatic carcinogenesis

Project description:Epigenetic reprogramming in hepatic carcinogenesis

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Hepatic transcriptomic changes during non-alcoholic steatohepatitis (NASH)-associated liver carcinogenesis in mice

Project description:Hepatocellular carcinoma (HCC), which accounts for 90% of all primary livers tumors, is the fourth most common cancer in the world. The development of HCC is a long-term and complex process, and uncovering the molecular mechanisms associated with HCC development is critical for the disease diagnosis, prevention, and treatment. Exploring these mechanisms using human HCC samples is desirable, but frequently impractical, with a number of limitations and shortcomings. The STAMTM (Stelic Institute & Co, Tokyo, Japan) mouse model of NASH-associated liver carcinogenesis is considered a useful and relevant model for investigating the molecular pathogenesis of NASH-derived HCC. This model resembles the human HCC development associated with progression from simple steatosis to NASH, fibrosis, and HCC. In the present study, by using high-throughput whole genome microarrays (SurePrint G3 Mouse Gene Expression v2, 8x60K; Agilent Technologies, Santa Clara, CA), we examined the transcriptomic profiles in the livers of STAMTM mice at different stages of liver carcinogenesis, including steatosis (6 week time interval), NASH (8 weeks), fibrotic stage (12 weeks), and in full-fledged HCC (20 weeks). The results of microarray analyses showed significant progressive changes in hepatic gene expression during the development of HCC. A total of 970, 1462, 2742, and 2857 of differentially expressed genes were identified in the livers at 6, 8, 12, and 20 weeks, respectively. Detailed analysis of these differentially expressed genes will benefit the understanding of the underlying mechanisms of non-alcoholic fatty liver disease-derived HCC.

2016-06-22 | GSE83596 | GEO

Hepatic transcriptomic changes during non-alcoholic steatohepatitis (NASH)-associated liver carcinogenesis in mice

2016-06-22 | E-GEOD-83596 | biostudies-arrayexpress

Transcription profiling of rodent hepatic carcinogenesis

Project description:3 dose levels of each of 9 compounds were used to dose male SD rats q.d. by oral gavage. Compounds included 5 nongenotoxic carcinogens (bemitradine, clofibrate, doxylamine, methapyrilene, & phenobarbital), 2 genotoxic agents (tamoxifen and 2-AAF) and 2 non-carcinogens (4-AAF and isoniazid). This work has been described in Kramer JA, Curtiss SW, Kolaja KL, Alden CA, Blomme EAG, Curtiss WC, Davila JC, Jackson CJ, and Bunch RT. (2004) Acute Molecular Markers of Rodent Hepatic Carcinogenesis Identified by Transcription Profiling. Chem. Res. Toxicol., in press.

2004-03-08 | E-MEXP-89 | biostudies-arrayexpress

Gene Expression Analysis Indicates Divergent Mechanisms in DEN-Induced Carcinogenesis in Wild Type and Bid-Deficient Livers

Project description:The aim of this study was to better understand the Bid-regulated events during hepatic carcinogenesis. The information from this set of data indicates that wild type and bid-deficient livers express different sets of genes after diethylnitrosamine (DEN) treatment.

2016-09-01 | GSE80488 | GEO

A diet enriched with biologically active substances as a protecting factor against carcinogenesis process induced by 1,2-dimethylhydrazine in rat liver

Project description:The aim of this study was to evaluate the ability of a diet enriched with biologically active compounds to protect against 1,2-dimethylhydrazine - induced carcinogenesis in 14-month old rats liver. Rats from control and experimental groups after 14 months of experiment were given 5 times 1,2-dimethylhydrazine (DMH) by intraperitoneal treatment at a dose of 30mg/kg of body weight once a week to induce the process of carcinogenesis. RNA from their livers were hybridized to Agilent two color microarrays with a common reference. Then, the transcriptomic profile of these livers were compared to the transcriptomic profile of 14-month rats received the same control diet and diet enriched with biologically active substances, but without 1,2-dimethylhydrazine - induction (data from GEO Submission - GSE51657).

2014-02-27 | E-GEOD-55378 | biostudies-arrayexpress

Hepatic gene expression after minipump bGH treatment of male rats

Project description:male young rats treated with bGH (minipumps for a week before RNA was prepared from livers Keywords: repeat sample

2005-05-04 | GSE2496 | GEO