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Liver tumor gene expression profile of liver-specific PTEN KO, PTEN/SCAP double KO mice

ABSTRACT: Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is characterized by hepatic steatosis and hepatocellular injury and progresss cirrhosis and hepatocellular carcinoma. Sterol regulatory elment-binding proteins (SREBPs) are master regulators of lipogenesis. Liver-specific PTEN knockout (KO) mice show constitutive upregulation of SREBP through PI3K-Akt pathway activation, leading to spontaneous fatty liver and subsequent HCC development. SREBP cleavage-activating protein (SCAP) plays a critical role in SREBP activation. We sought to determine the impact of SREBP inhibition on NASH and HCC development. To this end, we additionaly inhibited SREBP pathway in liver-specific PTEN mice by ablating SCAP and generated liver-specific PTEN/SCAP double KO (DKO) mice. However unexpectedly, inhibition of SCAP/SREBP pathway markedly exacerbated liver injury (5weeks), fibrosis (5months), and carcinogenesis (7 months) in PTEN KO mice. To elucidate the mechanisms of liver tumorigenesis in liver-specific PTEN/SCAP DKO mice, we conducted transcriptome analyses of the livers.

ORGANISM(S): Mus musculus

PROVIDER: GSE174173 | GEO | 2022/04/05

REPOSITORIES: GEO

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Liver gene expression profile of wild type, liver-specific PTEN KO, SCAP KO and PTEN/SCAP double KO mice.

Project description:Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is characterized by hepatic steatosis and hepatocellular injury and progresses to cirrhosis and hepatocellular carcinoma. Sterol regulatory element-binding proteins (SREBPs) are master regulators of lipogenesis. Liver-specific PTEN knockout (KO) mice show constitutive upregulation of SREBP through PI3K-Akt pathway activation, leading to spontaneous fatty liver and subsequent HCC development. SREBP cleavage-activating protein (SCAP) plays a critical role in SREBP activation. We sought to determine the impact of SREBP inhibition on NASH and HCC development. To this end, we additionally inhibited SREBP pathway in liver-specific PTEN mice by ablating SCAP and generated liver-specific PTEN/SCAP double KO (DKO) mice. However unexpectedly, inhibition of SCAP/SREBP pathway markedly exacerbated liver injury (5weeks), fibrosis (5months), and carcinogenesis (7 months) in PTEN KO mice. To elucidate the mechanisms of liver injury in liver-specific PTEN/SCAP DKO mice, we conducted transcriptome analyses of the livers.

2022-04-05 | GSE169104 | GEO

Liver gene expression profile of wild type, liver-specific PTEN KO, SCAP KO and PTEN/SCAP double KO mice.

Project description:Liver gene expression profile of wild type, liver-specific PTEN KO, SCAP KO and PTEN/SCAP double KO mice.

| PRJNA715216 | ENA

Liver tumor gene expression profile of liver-specific PTEN KO, PTEN/SCAP double KO mice

Project description:Liver tumor gene expression profile of liver-specific PTEN KO, PTEN/SCAP double KO mice

| PRJNA728674 | ENA

Genome-wide analysis of liver tissue mRNA expression from Pten-deficient and/or Sav1-deficient mice liver

Project description:To know the crosstalk between Hippo and AKT pathways in the liver metabolism, we generated liver-specific Pten (AKT signaling), Sav1 (Hippo signaling) and double-knockout mice and analysed the liver mRNA expression globally from 4groups (WT, Pten KO, Sav1 KO and Pten;Sav1 dKO).

2018-10-08 | GSE94797 | GEO

Mus musculus

Project description:Whole-exome sequencing of liver tumors developed in liver-specific PTEN KO mice and PTEN/SCAP double KO (DKO) mice.

| PRJDB11259 | ENA

Deletion of Scap in Alveolar Type II Cells Influences Lung Lipid Homeostasis and Identifies a Compensatory Role for Pulmonary Lipofibroblasts

Project description:Pulmonary function after birth is dependent upon surfactant lipids that reduce surface tension in the alveoli. The sterol-responsive element-binding proteins (SREBPs) are transcription factors regulating expression of genes controlling lipid homeostasis in many tissues. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo. Prior to birth (E18.5), deletion of Scap decreased the expression of both SREBPs and a number of genes regulating fatty acid and cholesterol metabolism. Nevertheless, Scap∆/∆ mice survived postnatally, surfactant and lung tissue lipids being substantially normalized in adult Scap∆/∆ mice. Although phospholipid synthesis was decreased in type II cells from adult Scap∆/∆ mice, lipid storage, synthesis, and transfer by lung lipofibroblasts were increased. mRNA microarray data indicated that SCAP influenced two major gene networks, one regulating lipid metabolism and the other stress-related responses. Deletion of the SCAP/SREBP pathway in respiratory epithelial cells altered lung lipid homeostasis and induced compensatory lipid accumulation and synthesis in lung lipofibroblasts. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo.Lung cRNA was hybridized to the murine genome MOE430 V2 chips.

2011-01-08 | E-GEOD-26496 | biostudies-arrayexpress

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Cv2]

Project description:The synthesis of fatty acids and cholesterol is regulated by three membrane-bound transcription factors: sterol regulatory element-binding proteins (SREBP)-1a, -1c, and -2. Their function in liver has been characterized in transgenic mice that overexpress each SREBP isoform and in mice that lack all three nuclear SREBPs because of gene knockout of SREBP cleavage-activating protein (SCAP) required for nuclear localization of SREBPs. Here, we use oligonucleotide arrays hybridized with RNA from livers of three lines of mice (transgenic for SREBP-1a, transgenic for SREBP-2, and knockout for SCAP) to identify genes that are likely to be direct targets of SREBPs in liver. Application of stringent combinatorial criteria to the transgenic/knockout approach allows identification of genes whose activities are likely controlled directly by the SREBPs.

2017-08-05 | GSE102258 | GEO

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Bv2]

2017-08-05 | GSE102257 | GEO

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Av2]

2017-08-05 | GSE102256 | GEO

Temporal gene expression patterns (Next Generation Sequencing) in liver tumourigenesis of hepatocyte-specific deletion of shp2 and/or pten

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to reveal dynamics of liver tumourigenesis in different mouse model and identify some key regulators that control HCC initiation or progression. We also try to define a index based on transcriptome of samples to quantify tumor development stage. Methods: mRNA profiles of wild-type (WT), hepatocyte-specific shp2 deletion (Shp2−/−) mice (SKO), hepatocyte-specific pten deletion (Pten−/−) mice (PKO), and hepatocyte-specific shp2 and pten deletion mice (DKO) were generated by deep sequencing. The sequence reads that passed quality filters were mapped to Mouse genome using STAR, and mRNA profiles were obtained using cuffdiff. Results: quanlity control of mRNA profiles showed that the data captured key features of phenotypes. Significantly changed genes, pathways, biolgocial processes, ligand and receptor, epigenetic regulators et al of SKO, PKO, DKO mice at differnet age were obtaiend. Temporal gene expression patterns during liver tumorigenesis in SKO, PKO and DKO mice were obtained. Conclusions: Our study represents the first detailed analysis of temporal transcriptomes during liver tumourigenesis, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comprehensive investigations of expression profiles.

2018-12-07 | GSE123427 | GEO

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