Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2882360_1.fastq.gz | Fastqsanger.gz | |||
| ERR2882360_2.fastq.gz | Fastqsanger.gz | |||
| ERR2882370_1.fastq.gz | Fastqsanger.gz | |||
| ERR2882370_2.fastq.gz | Fastqsanger.gz | |||
| ERR2882361_1.fastq.gz | Fastqsanger.gz |
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Project description:Peroxisome proliferator-activated receptor α (PPARA) is a key mediator of lipid metabolism and inflammation. Activation of PPARA in rodents causes hepatocyte proliferation, but the underlying mechanism is poorly understood. This study focused on genes repressed by PPARA and analyzed the mechanism by which PPARA promotes hepatocyte proliferation in mice. Activation of PPARA by agonist treatment was autoregulated, and induced expression of the epigenetic regulator UHRF1 via activation of the newly described PPARA target gene E2f8, that in turn regulates Uhrf1. UHRF1 strongly repressed expression of CDH1 via methylation of the Cdh1 promoter marked with H3K9me3. Repression of CDH1 by PPARA activation was reversed by PPARA deficiency or knockdown of E2F8 or UHRF1. Furthermore, forced expression of CDH1 inhibited expression of the Wnt signaling target genes such as Myc after PPARA activation, and suppressed hepatocyte hyperproliferation. These results demonstrate that the PPARA-E2F8-UHRF1-CDH1 axis causes epigenetic regulation of hepatocyte proliferation. This SuperSeries is composed of the SubSeries listed below.
2022-04-05 | GSE154277 | GEO
Project description:Cdh1 regulates not only mitotic phase and G1 phase, but also G2 checkpoint under irradiation-induced DNA damage. Despite several reports indicating its potential as tumor suppressor, how Cdh1 affects tumorigenesis or tumor progression and its clinical implementation has yet to be evaluated. Considering the pivotal role of Cdh1 on DNA repair, we hypothesized that Cdh1 loss also causes fragility of tumor cells to DNA damage under oncogenic stress or chemotherapy. To test this hypothesis, we established a Cdh1 gene-trapped B cell acute lymphoblastic leukemia (B-ALL) mouse model. Cdh1-deficient B-ALL mice survived longer than Cdh1-intact group, with higher susceptibility to DNA damage. Consistently, reverse phase protein array-based analysis of more than 200 human adult B-ALL samples showed that low Cdh1 was associated with high complete remission rates and long remission durations. Furthermore, the clinical benefit with lower Cdh1 expression diminished after relapse, supported by mouse experiments showing that secondary/tertiary transplants of Cdh1-deficient B-ALL cells developed more progressive/resistant disease than Cdh1-intact group. This indicated that prolonged inactivation of Cdh1 eventually develops resistant clones. Our results collectively demonstrated that Cdh1 is a potential predictive biomarker of B-ALL chemosensitivity, but also alerting that synthetic lethality by targeting DNA repair system may eventually induce resistant disease due to genetic instability.
2017-05-24 | GSE69863 | GEO
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
Project description:In this study, we wanted to explore the protein interactors of Cdh1, a subunit of the E3 Ubiquitin-Ligase Cdh1-APC. Our data show that in addition to interacting with other components of the Cdh1-APC complex, Cdh1 interacts with regulators of translation.
2020-04-29 | PXD018875 | Pride
Project description:RNA sequencing of CDH1+/THY1+ and CDH1-/THY1+ germline stem cells
| PRJNA355568 | ENA
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:Analysis of gene expression profile in Ras-induced senescent human diploid fibroblasts with or without depletion of fzr1/cdh1. Results provide insight into the effect on fzr1/cdh1 on the regulation of senescence-associated gene expression in human diploid fibroblasts. IMR-90-ER:Ras cells were cultured for 6 days with or without 4-hydroxytamoxifen (OHT) and were subsequently subjected to transfection with siRNA oligos against fzr1/cdh1 or control for three times (at 2 day intervals). Total RNA was isolated using Trizol reagent and were analyzed using the human 3D-Gene DNA chip (Toray) which that contains 25000 genes. The genome wide transcriptional response of proliferating cells (IMR si control2) and fzr1/cdh1 depleted senescent cells (IMR+OHT si cdh1) were compared to that of senescent cells (IMR+OHT si control).
2012-07-31 | E-GEOD-30790 | biostudies-arrayexpress
Project description:Three independent transcriptional profiling experiments were performed to ascertain how Dot1L affects cell fate change. 1) In a timecoure ("Tc"), reprogramming mouse embryonic fibroblasts were treated with DMSO control or Dot1L inhibitor (Dot1Li -SGC0946) for 2 or 4 days. Surprisingly, despite the enrichment of H3K79me2 on thousands of actively transcribed genes, Dot1L inhibition (Dot1Li) results in few changes in steady state mRNA levels during reprogramming, the majority of which are spuriously upregulated. 2) To determine if Dot1Li increased reprogramming beyond the mesenchymal to epithelial transition (MET) that occurs early in reprogramming when starting from MEFs, reprogramming cells were sorted ("Sort") for surface CDH1 expression, and then treated with Dot1Li or control. Dot1Li increased reprogramming efficiency of both CDH1- and CDH1+ populations to a similar extent and few genes were DE. 3) To assess if Dot1Li increased pluripotency acquisition beyond CDH1 upregulation, CDH1 or empty vector was expressed ("Exp") in reprogramming cells. CDH1 expression did not initiate MET, or enhance reprogramming.
2021-04-30 | GSE160580 | GEO
Project description:To analyze the effects of Cdh1 signaling on melanoma properties, we performed microarray analysis to identify genes induced by soluble Cdh1 in mouse melanoma cell line B16-F10.
2021-08-23 | GSE147154 | GEO