Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA208971 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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
Project description:Cdh1 and Trp53 Knockout organoid, Cdh1, Trp53 and Smad4 Knockout organoid RNA sequencing
| PRJNA902414 | ENA
Project description:To investigate the function of Smad4, we established Cdh1 and Trp53 Knockout organoid, Cdh1, Trp53 and Smad4 Knockout organoid lines We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.
2025-11-16 | GSE218151 | GEO
Project description:To identify the mechanisms driving resistance upon KrasG12V ablation, we established lung cancer cell lines that carried loxP sequences flanking the exon 1 of Kras containing the G12V mutation (Kras +/loxG12Vlox), and lacked Trp53 alleles (Trp53 -/-). Tumor cells were infected with Adeno-Cre particles to excise the floxed sequences and individual cells that survived were expanded for further analysis.
2023-03-05 | GSE204754 | GEO
Project description:The functional status of the tumor repressor protein (TP53 or TRP53) is a defining feature of ovarian cancer. Mutant or null alleles of TP53 are expressed in greater than 90% of all high-grade serous adenocarcinomas. Wild type TP53 is elevated in low-grade serous adenocarcinomas in women and in our Pten/Kras/Amhr2-Cre mutant mouse model. Disruption of the Trp53 gene in this mouse model did not lead to high-grade ovarian cancer but did increase expression of estrogen receptor alpha (ERalpha; ESR1) and markedly enhanced the responsiveness of these cells to estrogen. Specifically, when Trp53 positive and Trp53 null mutant mice were treated with estradiol or vehicle, only the Trp53 null and Esr1 positive tumors respond vigorously to estradiol in vivo and exhibit features characteristic of high-grade type ovarian cancer: invasive growth into the ovarian stroma, rampant metastases to the peritoneal cavity and signs of genomic instability. Estrogen promoted and progesterone suppressed the growth of Trp53 null ovarian tumors and tumor cells injected intraperitoneally (IP), subcutaneously (SC) or when grown in matrigel. Exposure of the Trp53 depleted cells to estrogen also has a profound impact on the tumor microenvironment and immune-related events. These results led to the new paradigm that TRP53 status is related to the susceptibility of transformed ovarian surface epithelial (OSE) cells to estradiol-induced metastases and genomic instability. This novel finding is relevant not only for women during their reproductive years but also for women on hormone (estradiol) replacement therapies. A direct comparison of ovarian surface epithelia cells from two different genotype mice
2014-03-21 | E-GEOD-51095 | biostudies-arrayexpress
Project description:Our findings establish a key role for the coregulator, Repressor of Estrogen receptor Activity (REA), in controlling the timing and magnitude of decidualization in human endometrial stromal cells in vitro and in the mouse uterus in vivo, and suggest that REA functions to synchronize uterine differentiation with concurrent embryo development, which is essential for optimal implantation and fertility. The findings highlight that REA physiologically restrains endometrial stromal cell decidualization, controlling the timing and magnitude of decidualization to enable proper synchronization of uterine differentiation with concurrent embryo development that is essential for implantation and optimal fertility.
2013-04-04 | GSE42376 | GEO
Project description:Loss of cell polarity and tissue disorganization occurs in majority of epithelial tumors. The role of cell polarity mechanisms in cancer is not completely understood. Here we analyzed the mammalian orthologs of drosophila apical-basal polarity gene lethal giant larvae (lgl), which also functions as a tumor suppressor in flies. There are two mammalian orthologs of lgl (Llgl1 and Llgl2). To determine the role of the entire Lgl signaling pathway in mammals we generated mice with ablation of both Llgl1 and Llgl2 in skin epidermis (Llgl1/2-/- cKO mice). Surprisingly, we found that ablation of Llgl1/2 does not impact epidermal polarity. However, old Llgl1/2-/- cKO mice develop skin lesions which are missing epidermal layer and ripe with inflammation. To determine the role of Llgl1/2 in cancer we generated Trp53-/-/Llgl1/2-/- and Trp53-/+/Llgl1/2-/- cKO mice. Loss of Llgl1/2 promoted squamous cell carcinoma (SCC) development in Trp53-/- cKO and caused SCC in Trp53-/+ cKO mice, while no cancer was observed in Trp53-/+ cKO controls. Mechanistically, we show that ablation of Llgl1/2 activates aPKC-NF-B-RelA signaling pathway and epidermis-specific deletion of only one allele of RelA rescues SCC phenotype in Trp53-/+/Llgl1/2-/- cKO mice. We conclude that Lgl signaling pathway functions as a tumor suppressor in mammalian skin.
2025-11-13 | GSE247772 | GEO
Project description:ChickenM-BM- ovalbumin upstream promoter-transcription factor II (COUP-TFII; NR2F2) is an orphan nuclear receptor involved in cell-fate specification, organogenesis, angiogenesis and metabolism. Ablation of COUP-TFII in the mouse uterus causes infertility due to defects in embryo attachment and impaired uterine stromal cell decidualization. Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown. To better elucidate the mechanisms with which COUP-TFII regulates target gene transcription, genome-wide COUP-TFII binding sites in human endometrial stromal cells (HESC) treated with deciduogenic hormones were identified using ChIP-seq. A total of 16,298 intervals (binding regions) for COUP-TFII were identified compared with the input in HESC chromatin with a very low false discovery rate (0.17%) using a stringent cutoff of p =1x10-10. Distribution of intervals showed that more than half (58.6%) of the COUP-TFII binding sites are located within 10 kb of gene boundaries. 7.5% of total intervals reside within the 10 kb promoter region. A total of 6,077 unique genes were identified to have COUP-TFII binding sites within 10 kb of their gene boundaries. Examination of NR2F2 binding in pooled primary human endometrial stromal cells from 6 healthy women upon decidualization with a hormone cocktail of cAMP, E2 and medroxyprogesterone acetate.
2013-11-02 | E-GEOD-52008 | biostudies-arrayexpress
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