Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The function of c-Fos in hepatocarcinogenesis

ABSTRACT: c-Fos, a member of the stress-activated Activator Protein 1 (AP-1) transcription factor family, is expressed in human hepatocellular cancer (HCC). Using genetically engineered mouse models (GEMMs) we show that hepatocyte-specific expression of c-Fos leads to a proliferative, de-differentiated phenotype, whereas hepatocyte-specific deletion of c-Fos protects against diethylnitrosamine (DEN)-induced liver cancer. Furthermore, c-Fos-expressing livers resemble human HCCs based on expression profiles. In the present RNA seq, we intend to analyze the transcriptomic profile of livers at 2 and 4 mo hepatocyte-specific c-Fos expression compared to the corresponding age-matched control mice. Moreover, we analyzed livers of mice with hepatocyte-specific deletion c-Fos at 48h after DEN treatment compared to identically treated control mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE81079 | GEO | 2017/03/23

SECONDARY ACCESSION(S): PRJNA320430

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiles of fractionated cells from cirrhotic rat livers

Project description:Gene expression profiling was performed in each of hepatocyte fraction and non-parenchymal cell fraction enriched with activated hepatic stellate cells/myofibroblasts from cirrhotic rat livers induced by repeated, low-dose diethylnitrosamine (DEN) treatment.

2016-12-16 | GSE63726 | GEO

Identification of HCC-specific genes in a rat model of hepatocarcinogenesis

Project description:The diethylnitrosamine HCC rat model (DEN-HCC) is a useful preclinical model mirroring human hepatocellular carcinoma. To overcome tumor heterogeneity of human HCCs linked to different etiologies and clonal selection, rat HCC samples were compared with matched non-tumor livers in order to identify HCC-related genes involved in the carcinogenetic process. Specifically, male Wistar rats received DEN (Sigma-Aldrich) in the drinking water (100 mg/L) for 8 weeks. Two weeks later the end of DEN treatment, animals were monitored by ultrasound imaging. Animals were euthanized 1 or 2 months after the end of DEN treatment, when the major diameter of at least one HCC nodule reached a dimension of 10 mm. Samples were collected for molecular biology and total RNA for microarray analysis was extracted by using Trizol. Two rat livers from untreated mice were included in the analysis.

2023-05-23 | E-MTAB-11977 | 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

Gene expression profiling of hepatocarcinogenesis initiation in Fischer-344 rats.

Project description:Diethylnitrosamine is used as initiator carcinogen in the modiffied resistan model but is not known its effect on gene expression profile on this stage. In other way, CAPE is compound with anticarcinogenic propertie when is administered 12 h before DEN and with the aim to characterize its effect on gene expression profile when is administered alone and in combination with diethylnitrosamine, these analysis were made. Male Fischer-344 rats were we used 4 animal per each treatment and all treatments are compared with not treated rats. Were identified groups of genes related with Carcinogens metabolism, oxidative stress and cell regulation with important differences between treatments.

2009-06-30 | GSE12030 | GEO

Gene expression profiling of hepatocarcinogenesis initiation in Fischer-344 rats.

2009-06-30 | E-GEOD-12030 | biostudies-arrayexpress

Context-specific roles of diphthamide deficiency in hepatocellular carcinogenesis

Project description:In our current study, we observed that in hepatic carcinogen diethylnitrosamine (DEN)-induced liver tumor mouse model, diphthamide-deficient mouse developed less liver tumor incidence than control mouse. To explore the detailed mechanism, RNA-seq experiment was conducted to compare gene transcriptome profiles of control and diphthamide-deficient livers during HCC progression.

2021-12-21 | GSE191192 | GEO

Genotoxicity of nitrosamines

Project description:We profiled the gene expression in eight chicken embryo livers in the 11th day of incubation. The eggs were injected on postincubation days 9, 10 and 11 with 4mg activation-dependent DNA reactive diethylnitrosamine (DEN) or its structural non-carcinogenic comparator, N-nitrosodiethanolamine (NDELA)DEN in 0.15 ml/egg deionized water. We found that both compounds induced simmilar massive transcriptomic alterations in the xenobioatic metabolism pathways when comparing with reference data in eggs injected with the vehicle only (deionized water).

2018-02-21 | GSE110906 | GEO

Astrocyte elevated gene-1 (AEG-1) promotes hepatocarcinogenesis: novel insights from a mouse model

Project description:Astrocyte elevated gene-1 (AEG-1) as a positive inducer of hepatocellular carcinoma (HCC). Transgenic mice with hepatocyte-specific expression of AEG-1 were challenged with N-nitrosodiethylamine (DEN) and developed multinodular HCC with steatotic features. Thus, we have identified the follwoing AEG-1 functions: induction of steatosis, inhibition of senescence and activation of coagulation pathway to augment an aggressive hepatocarcinogenic phenotype.

2012-07-25 | GSE34669 | GEO

Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [43MM]

Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples.

2012-08-08 | GSE39931 | GEO

Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [41MM]

2012-08-08 | GSE39930 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data