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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

ABSTRACT: Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation. A direct comparison of mouse uteri (n=3) from control, single ablation of Cdh1 or Trp53, and ablation of both Cdh1 and Trp53 at 2 months of age.

ORGANISM(S): Mus musculus

SUBMITTER: Kanako Hayashi

PROVIDER: E-GEOD-48131 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

Project description:Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation.

2014-06-23 | GSE48131 | 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

RNAi off-target analysis in Trp53-/- mouse embryonic fibroblasts transduced with miRNA-based shRNAs targeting Trp53.

Project description:We analyzed miRNA-based shRNA off-target effects by transducing Trp53-/- MEFs at single- and high-copy with six well-characterized, potent and weak Trp53 shRNAs. To advance RNAi therapy for KRAS-mutant cancer, we developed a functionally validated library of siRNAs against RAS pathway genes that minimize off-target effects and enable combination gene silencing at low dose. We developed an in vivo model for real-time tracking of nanoparticle-based siRNA delivery and offer proof-of-principle that siRNA-mediated inhibition of a single gene (KRAS) or combinations of genes (A/B/C-RAF or KRAS+PIK3C-A/B) can impair the growth of KRAS-mutant colorectal cancer xenografts. Trp53-/- MEFs were transduced with LMP expressing Trp53 shRNAs at single copy (11-21% infection efficiency) and high copy (>98% infection efficiency), selected on puromycin and grown in absence of the selection agent before harvest. Uninfected Trp53-/- MEFs and Trp53-/- MEFs infected with an empty vector control served as M-bM-^@M-^\no shRNAM-bM-^@M-^] reference.

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RNA sequencing of CDH1+/THY1+ and CDH1-/THY1+ germline stem cells

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2017-03-01 | GSE90712 | GEO

Mus musculus

Project description:Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

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Project description:NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

2024-01-31 | PXD048887 | Pride

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. 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.

2014-07-01 | E-GEOD-54234 | biostudies-arrayexpress

CDH1 knockout in mice

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Transcriptional profiling of Cdh1-associated genes in mouse melanoma.

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Cdh1 (Fzr1) Interactome in Neuroblastoma (N2A) cells

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