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Wnt secretion protein Evi/Gpr177 promotes glioma tumorigenesis

ABSTRACT: Silencing of Evi and beta-catenin in U87MG cells

ORGANISM(S): Homo sapiens

SUBMITTER: Iris Augustin

PROVIDER: E-MTAB-776 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Wnt secretion protein Evi/Gpr177 promotes glioma tumorigenesis

Project description:Silencing of Evi and beta-catenin in U87MG cells

| S-ECPF-MTAB-776 | biostudies-other

The Wnt secretion protein Evi/Gpr177 promotes glioma tumourigenesis.

Project description:Malignant astrocytomas are highly aggressive brain tumours with poor prognosis. While a number of structural genomic changes and dysregulation of signalling pathways in gliomas have been described, the identification of biomarkers and druggable targets remains an important task for novel diagnostic and therapeutic approaches. Here, we show that the Wnt-specific secretory protein Evi (also known as GPR177/Wntless/Sprinter) is overexpressed in astrocytic gliomas. Evi/Wls is a core Wnt signalling component and a specific regulator of pan-Wnt protein secretion, affecting both canonical and non-canonical signalling. We demonstrate that its depletion in glioma and glioma-derived stem-like cells led to decreased cell proliferation and apoptosis. Furthermore, Evi/Wls silencing in glioma cells reduced cell migration and the capacity to form tumours in vivo. We further show that Evi/Wls overexpression is sufficient to promote downstream Wnt signalling. Taken together, our study identifies Evi/Wls as an essential regulator of glioma tumourigenesis, identifying a pathway-specific protein trafficking factor as an oncogene and offering novel therapeutic options to interfere with the aberrant regulation of growth factors at the site of production.

| S-EPMC3306557 | biostudies-literature

Effect of Evi-1 deletion in hematopoietic stem cells

Project description:To identify the target genes of Evi-1 in hematopoietic stem cells (HSCs), we carried out genome-wide transcriptional analysis using wild-type and Evi-1-deleted HSCs.

2008-05-29 | GSE11557 | GEO

Structural Basis of WLS/Evi-Mediated Wnt Transport and Secretion.

Project description:Wnts are evolutionarily conserved ligands that signal at short range to regulate morphogenesis, cell fate, and stem cell renewal. The first and essential steps in Wnt secretion are their O-palmitoleation and subsequent loading onto the dedicated transporter Wntless/evenness interrupted (WLS/Evi). We report the 3.2 Å resolution cryogenic electron microscopy (cryo-EM) structure of palmitoleated human WNT8A in complex with WLS. This is accompanied by biochemical experiments to probe the physiological implications of the observed association. The WLS membrane domain has close structural homology to G protein-coupled receptors (GPCRs). A Wnt hairpin inserts into a conserved hydrophobic cavity in the GPCR-like domain, and the palmitoleate protrudes between two helices into the bilayer. A conformational switch of highly conserved residues on a separate Wnt hairpin might contribute to its transfer to receiving cells. This work provides molecular-level insights into a central mechanism in animal body plan development and stem cell biology.

| S-EPMC7797000 | biostudies-literature

Analysis of Evi-deficient teratoma

Project description:expression analysis of teratoma, grown from mouse embryonic stem cells that are Evi/Wls knockout cells and comparison with wildtype (control) tumors

2014-12-10 | E-MTAB-2927 | biostudies-arrayexpress

Transcription profiling of mouse Evi-1 deleted hematopoietic stem cells

Project description:To identify the target genes of Evi-1 in hematopoietic stem cells (HSCs), we carried out genome-wide transcriptional analysis using wild-type and Evi-1-deleted HSCs. Experiment Overall Design: Lineage(-), Sca-1(+), c-Kit(+) cells derived from Evi-1(flox/flox) mice were transduced with GFP or Cre-GFP expressing retroviruses. GFP(+) cells were sorted and and analyzed by AffymetrixÂ® Mouse Genome 430 2.0 ArrayÂ® for gene expression. Two independent experiments were performed.

2008-06-19 | E-GEOD-11557 | biostudies-arrayexpress

RNAseq transcriptomic signature associated depletion of Evi/Wls in epidermal sheets of mice, expression analysis of epidermal sheets of Evi/Wls knockout and wildtype mice

Project description:Evi/Wls is an essential Wnt secretion factor and important for tissue homeostasis. In the skin Wnt signaling plays an important role in hair follicle formation and maintenance. The aim of the present study is to compare the gene expression profile of Evi/Wls knockout epidermal sheets with wild-type control skin.

2013-07-24 | E-MTAB-1613 | biostudies-arrayexpress

Identification of endothelial genes co-regulated upon endothelial Evi/Wls and Rspo3 deletion

Project description:Inducible endothelial Rspo3 deletion resulted in perturbed developmental and tumor vascular remodeling. Rspo3-iECKO mice strikingly phenocopied the non-canonical WNT signaling-induced vascular defects of mice deleted for the WNT secretion factor Evi/Wls. An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified novel target genes, which could be linked to WNT/Ca2+/NFAT signaling. In summary, the study identifies endothelial RSPO3-driven non canonical WNT/Ca2+/NFAT signaling as critical maintenance pathway of the remodeling vasculature.

2016-02-03 | GSE75836 | GEO

Arrayexpression analysis of Evi-overexpressing teratomas

Project description:Canonical and non-canonical Wnt signaling play key roles during development and tumorigenesis. In this study we compared gene expression in teratomas grown from mouse embryonic stem cells that overexpress Evi/Wls and teratomas from normal embryonic stem cells cells.

2016-03-06 | E-MTAB-3995 | biostudies-arrayexpress

FoxM1 promotes ?-catenin nuclear localization and controls Wnt target-gene expression and glioma tumorigenesis.

Project description:Wnt/?-catenin signaling is essential for stem cell regulation and tumorigenesis, but its molecular mechanisms are not fully understood. Here, we report that FoxM1 is a downstream component of Wnt signaling and is critical for ?-catenin transcriptional function in tumor cells. Wnt3a increases the level and nuclear translocation of FoxM1, which binds directly to ?-catenin and enhances ?-catenin nuclear localization and transcriptional activity. Genetic deletion of FoxM1 in immortalized neural stem cells abolishes ?-catenin nuclear localization. FoxM1 mutations that disrupt the FoxM1-?-catenin interaction or FoxM1 nuclear import prevent ?-catenin nuclear accumulation in tumor cells. FoxM1-?-catenin interaction controls Wnt target gene expression, is required for glioma formation, and represents a mechanism for canonical Wnt signaling during tumorigenesis.

| S-EPMC3199318 | biostudies-literature

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