Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17903629_1.fastq.gz | Fastqsanger.gz |
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Project description:We report the induction of epithelial-mesenchymal transition (EMT) in the epithelial colorectal cancer (CRC) cell line DLD-1. ZEB2 expression is sufficient to induce the downregulation of epithelial markers such as E-cadherin, claudins, keratins and occludins, while upregulating the expression of several mesenchymal markers as vimentin and fibronectin.
2020-04-18 | GSE148823 | GEO
Project description:ZEB2-mediated EMT in CRC cell line DLD-1
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Project description:In order to comprehensively identify genes directly regulated by AP4, a genome-wide chromatin-immunoprecipitation analysis (ChIP) followed by next generation sequencing (ChIP-seq) was performed after activation of a conditional AP4 allele in DLD-1 cells. One DLD-1 Sample was sequenced.
2013-05-31 | E-GEOD-46935 | biostudies-arrayexpress
Project description:Systemic lupus erythematosus (SLE) damages multiple organs by producing various autoantibodies. Insufficient interleukin-2 (IL-2) production causes decreased regulatory T cells and permits expansion of autoreactive T cells in the development of SLE. We here show that decreased miR-200a-3p causes IL-2 hypoproduction through directly recruiting ZEB1 or ZEB2 and CtBP2 (ZEB1/ZEB2-CtBP2) complex in SLE T cells. First, we performed RNA sequencing with Illumina Hiseq to obtain the candidate miRNAs and mRNAs involved in the pathogenesis of SLE. We found that miR-200a-3p was significantly downregulated, while its putative targets, ZEB2 and CtBP2 were upregulated in CD4+ T cells in MRL/lpr lupus model mice compared with those of C57BL/6J control mice. ZEB1 and ZEB2 compose ZEB family and suppress various genes including IL-2 by recruiting CtBP2. IL-2 plays a critical role in immune tolerance and IL-2 defect has been recognized in SLE pathogenesis. Therefore, we hypothesized that decreased miR-200a-3p cause IL-2 defect through ZEB1/ZEB2-CtBP2 complex in SLE CD4+T cells. Overexpression of miR-200a-3p induced IL-2 production though downregulating ZEB1, ZEB2 and CtBP2 in EL4 cell lines. We further revealed that miR-200a-3p promote IL-2 expression by reducing the bindings of suppressive ZEB1/ZEB2-CtBP2 complex on NRE-A of IL-2 promoter in SLE murine T cells. Interestingly, ZEB1/ZEB2-CtBP2 complex on NRE-A (a negative regulatory element) were significantly upregulated after phorbol-12-myristate-13-acetate and ionomycin (PMA/Iono) stimulation in lupus T cells. Our findings provide a new insight for the epigenetic regulation of IL-2 defect in SLE.
2016-09-23 | GSE87219 | GEO
Project description:Here, we report that the Rho GTPase activators Vav2 and Vav3 utilize a new, miR-200c-dependent mechanism that maintains the epithelial state by limiting the abundance of the Zeb2 transcriptional repressor in breast cancer cells. In parallel, Vav proteins engage an expression program that maintains epithelial cell traits in 3D culture. Depletion of Vav proteins triggers EMT in epithelioid breast cancer cells and, conversely, expression of constitutively active Vav2 restores both miR-200c expression and epithelial traits in mesenchymal breast cancer cells. In silico analyses suggest that the negative Vav-Zeb2 axis is operative in human luminal breast tumors.
2018-09-21 | GSE97385 | GEO
Project description:Identification of mitotic BioLSF-interacting proteins whose association is sensitive to Factor Quinolinone Inhibitor 1 (FQI1): The dataset is comprised of two independent experimental replicates, with each biological replicate consisting of runs of 4 samples. For each set, the four protein samples were generated from cells in mitosis, in which cells lacked, expressed basal levels, or expressed induced levels of a biotinylated, tagged LSF protein (BioLSF). Finally, cells with induced BioLSF levels were treated for one hour in mitosis with either FQI1 or vehicle (DMSO). Proteins purified on streptavidin beads were analyzed by mass spectrometry. More specifically, the four runs in each set derived from: 1) DLD-1 Flp-In™ T-REx™ TIR1 parental cells treated with vehicle (Parent_DMSO) as a negative control, 2) DLD-1 Flp-In™ T-REx™ TIR1 BioLSF cells with only leaky, basal BioLSF expression (BioLSF_DMSO), 3) DLD-1 Flp-In™ T-REx™ TIR1 BioLSF cells with induced BioLSF expression (BioLSF_DOX), and 4) DLD-1 Flp-In™ T-REx™ TIR1 BioLSF cells with induced BioLSF expression that were treated with FQI1 in mitosis (BioLSF_DOX_FQI1).
2022-05-26 | PXD024149 | Pride
Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.
2021-03-23 | PXD022212 | Pride
Project description:Gene expression analysis of stable HMGA2-overexpressing DLD-1 cells (DLD-1-HMGA2) and its control cells (DLD-1-Vector).
2019-08-29 | GSE136544 | GEO
Project description:We performed RNA-seq to evaluated the transcriptional changes of CD73 knockdown in RD cells, a Fusion Negative Rhabdomyosarcoma cell line. We used a Dox-inducible shRNA targetting the 3'UTR of CD73 to knockdown this gene. Cells with No-Dox were used as control.
2024-02-07 | GSE240722 | GEO