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CDH1 knockout in mice

ABSTRACT: Employing Cre/loxP technology, a mouse model of liver specific Cdh1 (E-cadherin) depletion was created (fl/fl | +/wt). Previously, the mice had already been compared to littermates with normal Ecadherin levels (fl/fl | wt/wt), using a broad range of laboratory methods (Serum parameters, long-term weight analysis, histology, western blot, etc.). To analyze the effect of Cdh1 (E-Cadherin) depletion on the liver homeostasis on the RNA-level over the course of 3 time-points, liver tissue was aquired from mice groups aged 1 week, 3 weeks and 6 weeks. Mice with liver-specific Cdh1 depletion were compared to wildtype-like littermates. 1 week: n=2+2; 3 weeks: n=3+3; 6 weeks: n=3+3. Samples (mice) were not paired.

ORGANISM(S): Mus musculus

SUBMITTER: Stefan Krebs

PROVIDER: E-GEOD-54234 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Evidence for a role of E-cadherin in suppressing liver carcinogenesis in mice and men.

Schneider Marlon R MR Hiltwein Felix F Grill Jessica J Blum Helmut H Krebs Stefan S Klanner Andrea A Bauersachs Stefan S Bruns Christiane C Longerich Thomas T Horst David D Brandl Lydia L de Toni Enrico E Herbst Andreas A Kolligs Frank T FT

Carcinogenesis 20140519 8

The cell adhesion molecule E-cadherin has critical functions in development and carcinogenesis. Impaired expression of E-cadherin has been associated with disrupted tissue homeostasis, progression of cancer and a worse patient prognosis. So far, the role of E-cadherin in homeostasis and carcinogenesis of the liver is not well understood. By use of a mouse model with liver-specific deletion of E-cadherin and administration of the carcinogen diethylnitrosamine, we demonstrate that loss of E-cadher ...[more]

PMID: 24840851

Similar Datasets

CDH1 knockout in mice

Project description:Employing Cre/loxP technology, a mouse model of liver specific Cdh1 (E-cadherin) depletion was created (fl/fl | +/wt). Previously, the mice had already been compared to littermates with normal Ecadherin levels (fl/fl | wt/wt), using a broad range of laboratory methods (Serum parameters, long-term weight analysis, histology, western blot, etc.). To analyze the effect of Cdh1 (E-Cadherin) depletion on the liver homeostasis on the RNA-level over the course of 3 time-points, liver tissue was aquired from mice groups aged 1 week, 3 weeks and 6 weeks.

2014-07-01 | GSE54234 | GEO

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

Transcriptome sequencing of tumor associated macrophages cells in HCC liver of OXCT1mKO mice.

Project description:6-8 weeks male LysCre/+ OXCT1fl/fl (OXCT1mKO or mKO for short) and its littermates Lys+/+ OXCT1fl/fl (control or ctrl) mice were used to build HCC implantation model (Hep1-6 in Portal Vein injection). RNA was extracted from tumor associated macrophages of OXCT1mKO and their littermate control mice for transcriptome analysis of macrophage function.

2024-07-21 | GSE237917 | GEO

Modeling, dissecting, and subtyping of E-cadherin inactivation-associated diffuse-type gastric adenocarcinoma

Project description:Diffuse-type gastric adenocarcinoma (DGAC) is lethal cancer that is often diagnosed late and resistant to therapeutics. Although hereditary DGAC is mainly characterized by mutations in the CDH1 gene that encodes E-cadherin, the impact of E-cadherin inactivation in DGAC tumorigenesis remains unclear. To address this, we established and characterized a CDH1 loss-associated DGAC model system with a human DGAC single-cell transcriptome. We genetically engineered murine gastric organoids (GOs; Cdh1 KO, KrasG12D, Trp53 KO [EKP]) that recapitulates human DGAC tumorigenesis. Cdh1 depletion is sufficient to 1. Single-cell transcriptomics of human DGAC datasets classified patients into three subtypes (DGAC1, 2, and 3). By transcriptional signature, EKP GOs belong to the DGAC1 subtype displaying CDH1 downregulation and epithelial-mesenchymal transition. Compared to DGAC2 and DGAC3, the DGAC1 subtype was characterized by T cell exhaustion, PILRA-CD99 enrichment, and potential sensitivity to PD1 inhibitors. Additionally, we identified the EZH2-mediated transcriptional circuit as a key regulon specifically activated in EKP and a therapeutic vulnerability. This study unravels the unexpected role of E-cadherin loss in cell lineage plasticity, transcriptional reprogramming, and immune evasion of DGAC and further stratifies DGAC patients by single-cell transcriptomics, providing novel insights into E-cadherin loss-associated DGAC tumorigenesis.

2023-08-07 | GSE226266 | GEO

Whole Exome Sequencing of Signet Ring/Plasmacytoid Variant Bladder Cancer

Project description:<p>In this study, six plasmacytoid bladder cancers were analyzed by whole exome sequencing. The results show loss of the CDH1 gene in every sample and correlate with E-cadherin loss of expression by immunohistochemistry. A separate validation cohort of plasmacytoid samples showed loss of E-cadherin expression by CDH1 mutation or promoter hypermethylation.</p>

| phs001064 | dbGaP

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls. mRNA was extracted from 100mg mouse liver samples and hybridized to Affymetrix microarrays. For each group (HDAC3 depleted liver and normal liver), we have 5 samples from different mice.

2011-03-11 | E-GEOD-25937 | biostudies-arrayexpress

Splicing Factor SRSF1 Deficiency in the Liver Triggers NASH-like Pathology via R-Loop Induced DNA Damage and Cell Death

Project description:Regulation of RNA processing contributes profoundly to tissue development and physiology. The serine-arginine-rich splicing factor 1 (SRSF1) is essential for hepatocyte function and survival. Although SRSF1 is mainly known for its many roles in mRNA metabolism, it is also crucial for maintaining genome stability. We show that acute liver damage in the setting of targeted SRSF1 deletion in mice is primarily mediated by the excessive formation of deleterious RNA–DNA hybrids (R-loops), which induce DNA damage. Combining hepatocyte-specific transcriptome, proteome, and RNA binding analyses, we demonstrate that widespread genotoxic stress following SRSF1 depletion results in global inhibition of mRNA transcription and protein synthesis, leading to impaired metabolism and trafficking of lipids. Accumulation of lipids in SRSF1-deficient hepatocytes is quickly followed by necroptotic cell death, inflammation, and fibrosis, resulting in NASH-like liver pathology. This pathogenesis is recapitulated in SRSF1-depleted human liver cancer cells illustrating a conserved and fundamental role for SRSF1 in preserving genome integrity and tissue homeostasis. This data set contains a proteomic comparison of hepatocytes from wild type vs. acute knockout of SRSF1. The acute knockout was generated by injecting 8-week-old SRSF1 fl/fl mice with a viral vector expressing Cre under the control of the liver-specific thyroxine binding globulin (TBG) promoter (AAV8-TBG-iCre). Controls were generated by injecting AAV8-TBG-GFP viral vector. The hepatocytes were isolated 2 weeks post injection.

2023-03-11 | PXD027035 | Pride

Gene expression in mouse liver depleted of HDAC3

2011-03-11 | GSE25937 | GEO

Polysome profiling analysis of myeloid progenitors of control mice or mice conditionally deficient for Elp3 in the hematopoietic system

Project description:Aim of the experiment was to compare the genes enriched in the heavy polysome fraction of myeloid progenitors originating from control Elp3fl/fl mice, and in myeloid progenitors originating from mice that underwent hematopoietic cell-restricted deletion of the catalytic subunit Elp3 of the Elongator complex (Elp3HscKO mice). The Elp3fl/fl strain was generated in house and first described in (DOI: 10.1084/jem.20142288). Littermates of 8-12 weeks old were used in all experiments.

2020-12-10 | E-MTAB-9628 | biostudies-arrayexpress

Ileum single cells expression in mice lacking Pgc1α in the intestine in response to western diet feeding.

Project description:To generate iPGC1α-/- mice, PGC1αfl/fl mice were intercrossed with Vil1-Cre mice to obatin Vil1-CreTg/-PGC1αfl/- mice. These mice were then backcrossed with PGC1αfl/fl mice to restore homozygosity for the iPGC1α floxed allele. Male Vil1-CreTg/-PGC1αfl/fl mice were bred to PGC1αfl/fl to produce the mice used in the study. PGC1αfl/fl (iPGC1afl/fl) littermates were used as controls.

2023-11-02 | GSE227610 | GEO

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