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Microarray analysis of WT, SKO, PKO and DKO liver samples

ABSTRACT: Microarray analysis of WT (Pten2fl/fl:Shp2fl/fl:Alb-Cre-), SKO (Shp2hep-/-, or Shp2fl/fl:Alb-Cre+), PKO (Ptenhep-/-, or Pten2fl/fl:Alb-Cre+) and DKO (Ptenfl/fl:Shp2fl/fl:Alb-Cre+) liver samples to gain global molecular insights how shp2 and pten is involved in liver tumorigenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE74732 | GEO | 2016/12/13

SECONDARY ACCESSION(S): PRJNA301360

REPOSITORIES: GEO

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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

RNA sequencing of wildtype, PTEN single knockout (SKO), and PTEN;Rb1 double knockout (DKO) mouse prostate organoids

Project description:The goal of this study was to perform transcriptomics on wildtype, PTEN single knockout (SKO) and PTEN;Rb1 double knockout (DKO) mouse prostate organoids. We isolated basal cells from PTEN floxed and PTEN;Rb1 floxed mouse prostates and infected with either RFP control or Cre recombinase to establish wildtype, SKO, and DKO mouse prostate organoids.

2023-09-01 | GSE221020 | GEO

Differential gene expression of mouse liver samples after poly I:C treatment

Project description:To understand differential gene expression globally with/without poly I:C treatment on liver cancer mouse model, RNA-seq analysis were examined using diethlynitrosamine-induced Shp2∆H (Shp2F/F:Alb-cre) and Pten∆H (PtenF/F:Alb-cre) mice.

2017-10-25 | GSE95782 | GEO

IκBζ Regulates the Development of Nonalcoholic Fatty Liver Disease through the Attenuation of Hepatic Steatosis in Mice

Project description:IκBζ is a transcriptional regulator that augments inflammatory responses from the Toll-like receptor or interleukin signaling. These innate immune responses contribute to the progression of nonalcoholic fatty liver disease (NAFLD); however, the role of IκBζ in the pathogenesis of NAFLD remains elusive. We investigated whether IκBζ was involved in the progression of NAFLD in mice. We generated hepatocyte-specific IκBζ-deficient mice (Alb-Cre; Nfkbizfl/fl) by crossing Nfkbizfl/fl mice with Alb-Cre transgenic mice. NAFLD was induced by feeding the mice a choline-deﬁcient, L-amino acid-deﬁned, high-fat diet (CDAHFD). CDAHFD-induced IκBζ expression in the liver was observed in Nfkbizfl/fl mice, but not in Alb-Cre; Nfkbizfl/fl mice. Contrary to our initial expectation, IκBζ deletion in hepatocytes accelerated the progression of NAFLD after CDAHFD treatment. Although the increased expression of inflammatory cytokines and apoptosis-related proteins by CDAHFD remained unchanged between Nfkbizfl/fl and Alb-Cre; Nfkbizfl/fl mice, early-stage steatosis of the liver was significantly augmented in Alb-Cre; Nfkbizfl/fl mice. Overexpression of IκBζ in hepatocytes via the adeno-associated virus vector attenuated liver steatosis caused by the CDAHFD in wild-type C57BL/6 mice. This preventive effect of IκBζ overexpression on steatosis was not observed without transcriptional activity. Microarray analysis revealed a correlation between IκBζ expression and the changes of factors related to triglyceride biosynthesis and lipoprotein uptake. Our data suggest that hepatic IκBζ attenuates the progression of NAFLD possibly through the regulation of the factors related to triglyceride metabolism.

2022-06-05 | GSE205390 | GEO

Comprehensive proteometics identifies FBXL6 substrates involved in liver cancer

Project description:FBXL6 is frequently over-expressed in human hepatocellular carcinoma (HCC). However, it is still unknown the underlying mechanisms by which FBXL6 promotes HCC. In this study, we compared ubiquitinated protein profiles among a panel of liver tissue samples (including HCC, adjacent tissues and normal tissues) from Fbxl6LSL-fl/+; Alb-cre mice and Alb-cre mice by proteomics and ubiquitomics analysis. There are many proteins with ubiquitination in FBXL6 overexpressed HCC, suggesting ubiquitination may play a critical role in FBXL6-mediated HCC. A1--- normal tissue 1 A2--- normal tissue 2 B1--- Adjacent tissue 1 B2--- Adjacent tissue 2 C1--- HCC tissue 1 C2--- HCC tissue 2

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Differential gene expression pattern of mouse livers transfected with dual oncogenes (day-3 post-injection data set)

Project description:To understand global gene expression patterns of mouse livers upon dual-oncogene transfection, RNA sequencing and analysis were conducted on liver samples from Shp2F/F or Shp2∆H (Shp2F/F:Alb-cre) mice hydrodynamically injected with the combination of Met/β-Catenin or Met/PIK3CA .

2017-04-25 | GSE97996 | GEO

Differential gene expression pattern of mouse livers transfected with dual oncogenes (day-7 post-injection data set)

2018-01-25 | GSE109544 | GEO

Met Expression Signature in Hepatocytes

Project description:To identify HGF/Met regulated genes, we performed expression microarray analysis after inducible activation of Met receptor in primary cultures of hepatocytes established from wild-type control (Alb-Cre +/-) and Met conditional knockout mice (Alb-Cre +/-; Met Fl/Fl). Keywords: time series design

2006-10-02 | GSE4451 | GEO

The potential biomarkers for HCC patients with functional loss of both p53 and Tsc1

Project description:p53 mutations occur frequently in human hepatocellular carcinoma (HCC). Activation of the mammalian target of rapamycin (mTOR) pathway is also associated with HCC. However, it is still unknown whether these changes together initiate HCC and can be targeted as a potential therapeutic strategy. Here, we compared transcriptional profiles among a panel of liver tissue samples from p53+/-, Tsc1fl/fl;Alb-cre, and p53+/-;Tsc1fl/fl;Alb-cre mice by RNAseq analysis. The overlapping genes in those three genotypes were considered potential biomarkers for HCC patients with functional loss of both p53 and Tsc1.

2021-08-30 | GSE153223 | GEO

Hepatic transcriptome analysis of PRDX1fl/fl and Alb-Cre；PRDX1fl/fl mice on MCD

Project description:The etiology of non-alcoholic steatohepatitis (NASH) has been complicated. An increasing body of literature has indicated that hepatic oxidative stress exerts a causal role in driving NASH. Nevertheless, how the anti-oxidant defense system guards against oxidative stress and NASH remains unclear. In this study, we sought to investigate how the peroxidase peroxiredoxin 1 protects against NASH. To this end, we fed WT and hepatic PRDX1 knockout (Alb-Cre;Prdx1fl/fl) a methionine and choline deficient diet (MCD) for 5 weeks and collected liver samples for RNA sequencing analysis. As revealed by gene-set enrichment analysis (GSEA) and KEGG pathway enrichment analysis, there was an enrichment of genes involved in JAK-STAT signaling. Further, we observed that the expression of many genes involved in JAK-STAT signaling such as Pdgfb and Pdgfra was significantly increased in Alb-Cre;Prdx1fl/fl mice. Collectively, these results suggest that increased JAK-STAT signaling accounts for the deteriorated NASH phenotypes in Alb-Cre;Prdx1fl/fl mice.

2023-08-14 | GSE201030 | GEO

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