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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.

ORGANISM(S): Mus musculus

PROVIDER: GSE48131 | GEO | 2014/06/23

SECONDARY ACCESSION(S): PRJNA208971

REPOSITORIES: GEO

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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. 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.

2014-06-23 | E-GEOD-48131 | biostudies-arrayexpress

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

Genome-wide Profiling of FOXA2 and POL2 binding in the mouse uterus [ChIP-Seq]

Project description:Forkhead box A2 (FOXA2) is a critical regulator of endometrial gland development in mice. In the adult mouse uterus, FOXA2 is expressed solely in the GE cells of the endometrium. Conditional deletion of Foxa2 after birth in the uterus, using the progesterone receptor Cre mouse (PgrCre), impeded gland development, thereby rendering the adult mouse infertile due to defects in blastocyst implantation stemming from a lack of endometrial glands and their secretions. As a first step to begin understanding the FOXA2 function in the endometrial glands of the uterus, genome-wide investigation of in vivo FOXA2 and RNA polymerase II (POL2) binding target regions in the neonatal and adult uterus was determined by chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-Seq). In order to determine the transcriptional regulatory networks mediating FOXA2 regulation of endometrial gland development and function, chromatin immunoprecipitation and massively parallel sequencing (ChIP-Seq) was used to create a genome-wide profile of in vivo FOXA2-binding sites in the developing (PD 12) and adult (DOPP 2.5 and 3.5) mouse uterus.

2013-12-01 | E-GEOD-48238 | biostudies-arrayexpress

Genome-wide Profiling of FOXA2 and POL2 binding in the mouse uterus [ChIP-Seq]

2013-12-01 | GSE48238 | GEO

Analysis of Porcupine ablation within the uterine epithelium on gene expression within the uterus

Project description:The secretion of mammalian Wnt Ligands within the cell is dependent on the activity of Porcupine, a gene located on the X chromosome that encodes for a membrane bound o-acyl transferase. Porcupine-dependent Wnt signalling was previously shown to be essential for the post-natal maintenance of endometrial glands, structures that are essential for implantation and fertility. Previous data has implicated the multiple members of the Wnt family expressed in the female uterus to be involved in a coordinated crosstalk between the luminal and stromal compartments of the uterus, ensuring the proper development of the uterus and successful fertility. We have generated a conditional mutant of Porcupine in the luminal epithelium (cKOepi) of the uterus, thus eliminating Wnt7a/b and Wnt11, to address the nature of this crosstalk. Unlike global luminal-stromal mutants, post-natal ablation of Porcupine in the luminal epithelium alone does not affect the maintenance of the endometrial glands in adults. Uterine glands are still visible in the adult cKOepi, albeit in a smaller number than that of control uteri. Despite having uterine glands, cKOepi females remain completely infertile. We have attributed the sterility of these females to be in part due to defects in implantation and decidualization; cKOepi fail to respond to decidual induction by artificial means. Interestingly, progesterone supplementation rescues the observed implantation defects, although observed decidual soon seem to become resorptive. Microarray analysis of cKOepi during implantation has reveals several potential targets for luminal WNT that may be responsible for the observed phenotype including: Lef1, Hoxa10, Wnt4, Wnt16 Notch1, Notch4 and Dll4 .

2017-03-21 | GSE96801 | GEO

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

Project description:To futher understand the properties of CDH1+ GSCs and CDH1- GSCs, flow cytometry was used to sort the twopopulations after trypsin digestion and they were compared by total RNA sequencing (RNA-seq). The data clearlyshowed CDH1+ and CDH1- cells as having highly distinct profiles. In particular, numerous epithelial genes (e.g.Dsp, Pkp2, Krt19) were highly expressed in the CDH1+ population. In contrast, most genes known to be generalmarkers of SSCs/undifferentiated spermatogonia were downregulated (e.g. GFRA1 and ID4) or unchanged (e.g. ZBTB16and SALL4) in CDH1- GSCs. Additionally, KEGG pathway analysis revealed that the two populations exhibiteddistinctive activity in several signaling pathways including WNT and TGFb signaling. Notably, Tgfbr1, Smad2, Smad3tended to be lower in CDH1+ GSCs while Smad7, an inhibitor of TGFb signaling, was higher.The results showed thatCDH1+ GSCs were more epithelial in nature compared to CDH1- GSCs and supported the notion that CDH1+ GSCs are areable to partly overcome MET barrier because they may be in an advanced stage of MET.

2017-03-01 | GSE90712 | GEO

Loss of Cdh1 and Trp53 in the uterus induces chronic inflammation with modification of tumor microenvironment.

Project description: Not available

| S-EPMC4551401 | biostudies-literature

Mus musculus

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

| PRJNA208971 | ENA

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

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

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