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

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

PROVIDER: PRJNA508735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8285550.fastq.gz	Fastqsanger.gz
	SRR8285560.fastq.gz	Fastqsanger.gz
	SRR8285570.fastq.gz	Fastqsanger.gz
	SRR8285580.fastq.gz	Fastqsanger.gz
	SRR8285590.fastq.gz	Fastqsanger.gz

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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

Microarray of wild type, Shp2 knock-out, Pten knock-out and double knock-out erythroblasts

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2013-07-03 | E-GEOD-48477 | biostudies-arrayexpress

Microarray of wild type, Shp2 knock-out, Pten knock-out and double knock-out erythroblasts

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Hepatocyte-specific knockout of Pten and of Pten and Tgfbr2 in mice

Project description:Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression Gene expression of the following mouse livers were characterized A. WT (n=3). B. Pten-/- (n=4). C. Pten-/- Tgfbr2-/- (n=4).

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Project description:1205Lu Metastatic Human melanoma cell lines with knockdown of Shp2 (PTPN11) were grown as xenograft tumors in NSG mice. RNA was extracted from the tumors and analyzed on [HuGene-2_0-st] Affymetrix Human Gene 2.0 ST Array [transcript (gene) version] Shp2 knockdown compared with non-target controls

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Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the breast cancer cells BT474 grown as xenografts in the presence or absence of SHP2 for 30 days. The HER2-postive breast cancer cell line BT474 was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in imuunodeficinet mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.

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2012-01-16 | E-GEOD-35118 | biostudies-arrayexpress

SHP2 inhibitor augments murine liver regeneration via cytoprotective and proproliferative pathway enhancement identified by RNA sequencing

Project description:Disruption of the liver’s innate ability to regenerate represents an “undruggable” clinical challenge associated with poor patient outcomes. Yes-associated protein (YAP), a transcriptional co-activator which is repressed by the Hippo pathway, is instrumental in liver regeneration. We have previously described an alternative, Hippo-independent activation of YAP mediated by tyrosine-protein phosphatase non-receptor type 11 (SHP2) inhibition. Herein, we examined the effects of YAP activation with a selective SHP1/SHP2 inhibitor, NSC-87877, on liver regeneration in murine partial hepatectomy models. In our studies, NSC-87877 led to accelerated hepatocyte proliferation, improved liver regeneration, and decreased markers of injury following partial hepatectomy. Evaluation of these effects in mice with hepatocyte-specific Yap/Taz deletion demonstrated dependence on these molecules for the enhanced regenerative response. Furthermore, administration of NSC-87877 to murine models of non-alcoholic steatohepatitis was associated with improved survival and decreased markers of injury post-hepatectomy. Evaluation of transcriptomic changes in the context of NSC-87877 administration revealed reduction in fibrotic signaling and augmentation of cell cycle signaling. Cytoprotective changes included downregulation of Nr4a1, an apoptosis inducer. Collectively, the data suggest that SHP2 inhibition induce a YAP-dependent pro-proliferative and cytoprotective enhancement of liver regeneration.

2022-03-17 | GSE198641 | GEO

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