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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Astrocyte elevated gene-1 (AEG-1) and c-Myc cooperate to promote hepatocarcinogenesis

ABSTRACT: Double transgenic mice with hepatocyte-specific expression of AEG-1 and c-Myc show aggressive HCC compared to single transgenics. Gene expression was analyzed to understand the molecular mechanism by which AEG-1 and c-Myc cooperate to promote hepatocarcinogenesis. Livers were collected from naïve adult mice (3 mice/group). Total RNA was extrancted and subjected to RNA-Seq.

ORGANISM(S): Mus musculus

SUBMITTER: Hung-I Chen

PROVIDER: E-GEOD-61875 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Astrocyte elevated gene-1 and c-Myc cooperate to promote hepatocarcinogenesis in mice.

Srivastava Jyoti J Siddiq Ayesha A Gredler Rachel R Shen Xue-Ning XN Rajasekaran Devaraja D Robertson Chadia L CL Subler Mark A MA Windle Jolene J JJ Dumur Catherine I CI Mukhopadhyay Nitai D ND Garcia Dawn D Lai Zhao Z Chen Yidong Y Balaji Uthra U Fisher Paul B PB Sarkar Devanand D

Hepatology (Baltimore, Md.) 20150123 3

<h4>Unlabelled</h4>Astrocyte elevated gene-1 (AEG-1) and c-Myc are overexpressed in human hepatocellular carcinoma (HCC) functioning as oncogenes. AEG-1 is transcriptionally regulated by c-Myc, and AEG-1 itself induces c-Myc by activating the Wnt/β-catenin-signaling pathway. We now document the cooperation of AEG-1 and c-Myc in promoting hepatocarcinogenesis by analyzing hepatocyte-specific transgenic mice expressing either AEG-1 (albumin [Alb]/AEG-1), c-Myc (Alb/c-Myc), or both (Alb/AEG-1/c-Myc ...[more]

PMID: 25065684

Similar Datasets

Astrocyte elevated gene-1 (AEG-1) and c-Myc cooperate to promote hepatocarcinogenesis

Project description:Double transgenic mice with hepatocyte-specific expression of AEG-1 and c-Myc show aggressive HCC compared to single transgenics. Gene expression was analyzed to understand the molecular mechanism by which AEG-1 and c-Myc cooperate to promote hepatocarcinogenesis.

2014-09-30 | GSE61875 | 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. Transgenic Mice liver tumors compared against WT mice liver tumors.

2012-07-24 | E-GEOD-34669 | biostudies-arrayexpress

Astrocyte elevated gene-1 and c-Myc cooperate to promote hepatocarcinogenesis in mice.

Project description: Not available

| S-EPMC4309751 | biostudies-other

Astrocyte elevated gene-1 promotes hepatocarcinogenesis: novel insights from a mouse model.

Project description: Not available

| S-EPMC3449036 | biostudies-literature

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

2012-07-25 | GSE34669 | GEO

Expression data from Wild-type (WT) and Alb/AEG-1 mice which are transgenic mice with hepatocyte-specific overexpression of AEG-1 (Astrocyte elevated gene 1)

Project description:AEG-1 is overexpressed in human hepatocellular carcinoma (HCC) and positively regulates development and progression of HCC A transgenic mouse with hepatocyte-specific expression of human AEG-1 was generated using mouse albumin promoter/enhancer in B6/CBA background. Hepatocytes were isolated from WT and Alb/AEG-1 mice for RNA extraction and Affymetrix microarray hybridization.

2013-07-01 | E-GEOD-46701 | biostudies-arrayexpress

FGF19 and its analog Aldafermin cooperate with MYC to induce aggressive hepatocarcinogenesis

Project description:Fibroblast growth factor 19 (FGF19) gene amplification is a common event in human hepatocellular carcinoma (HCC). The protein it encodes acts as a hormone with multiple metabolic functions beneficial for the liver, which has led to the development of analogues for the treatment of metabolic disorders such as Nonalcoholic Steatohepatitis (NASH). The most studied analogue is Aldafermin (NGM282), with previous reports showing the absence of oncogenic properties when given alone. However, potential oncogenic cooperation with frequent disrupted pathways in HCC have not been studied. Here, we used hydrodynamic gene transfer and recombinant protein injection to study oncogenic cooperation between FGF19 and its rodent orthologue FGF15, FGF19 analogue Aldafermin and common HCC events. We found a strong cooperation between FGF15/19 or Aldafermin and hepatocyte overexpression of Myc. The resulting tumours appeared in a short frame (2 to 4 weeks), were well differentiated, and expressed typical HCC markers (alpha foetoprotein and glypican 3). Transcriptomic and pathological analyses showed that Myc/FGF19 and Myc/Aldafermin tumours were almost identical. Our findings could be clinically relevant since clinical studies are currently ongoing in patients with cirrhosis, a condition associated with high susceptibility to HCC development.

2023-12-18 | GSE242953 | GEO

FtsH12 abundance modulates chloroplast development in Arabidopsis thalian

Project description:Proteomic investigation of Arabidopsis thaliana ftsH12 - ftsH12 is one of 17 genes of the FtsH metallo-protease family encoded within the A. thaliana genome.

2020-11-25 | PXD010615 | Pride

MYC-driven mouse HCC proteomics

Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").

2022-10-12 | PXD031478 | Pride

MMTV-Myc tumor development in E2F-null backgrounds

Project description:Advances in genomic signatures have begun to dissect breast cancer heterogeneity, and application of these signatures will allow the prediction of which pathways are important in tumor development. Here we used genomic signatures to predict involvement of specific E2F transcription factors in Myc-induced tumors. We genetically tested this prediction by interbreeding Myc transgenics with mice lacking various activator E2F alleles. Tumor latency decreased in the E2F1 mutant background and significantly increased in both the E2F2 and E2F3 mutants. Investigating the mechanism behind these changes revealed a reduction in apoptosis in the E2F1 knockout strain. E2F2 and E2F3 mutant backgrounds alleviated Myc effects on the mammary gland, reducing the susceptible tumor target population. Gene expression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with EMT, corresponding with a reduction in probability of Ras activation. In human breast cancer we found that a low probability of E2F2 pathway activation was associated with increased relapse-free survival time. Together these data illustrate the predictive utility of genomic signatures in deciphering the heterogeneity within breast cancer and illustrate the unique genetic requirements for individual E2Fs in mediating tumorigenesis in both mouse models and human breast cancer. MMTV-Myc tumors were generated in an E2F wild-type, E2F1 null, E2F2 null and E2F3 heterozygous background. When the primary tumor reached the endpoint, the tumors were flash frozen. 20 tumors from each genotype were selected for microarray analysis.

2011-12-29 | E-GEOD-24594 | biostudies-arrayexpress

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