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CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

ABSTRACT: High-grade glioma is highly aggressive and malignant, resistant to combined therapies and easy to relapse. A better understanding of circRNA biological function in high-grade glioma might contribute to the therapeutic efficacy. Here, a circRNA merely up-regulated in high-grade glioma, circGLIS3 (hsa_circ_0002874, originating from exon 2 of GLIS3), was validated by microarray and qRT-PCR. Functional experiments uncovered that up-regulation of circGLIS3 promoted glioma cell migration and invasion, and showed aggressive characteristics in tumor-bearing mice. Fluorescence in situ hybridization, RNA pull-down, RNA immunoprecipitation and immunohistochemical staining showed that circGLIS3 could promoted Ezrin T567 phosphorylation. Further investigation showed that circGLIS3 could be excreted by glioma through exosomes and induced endothelial cells angiogenesis. This study indicates that circGLIS3 is up-regulated in high-grade glioma and contributes to the invasion and angiogenesis of glioma via promoting Ezrin T567 phosphorylation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165926 | GEO | 2021/09/22

REPOSITORIES: GEO

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CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

Project description:High-grade glioma is highly aggressive and malignant, resistant to combined therapies and easy to relapse. A better understanding of circRNA biological function in high-grade glioma might contribute to the therapeutic efficacy. Here, a circRNA merely up-regulated in high-grade glioma, circGLIS3 (hsa_circ_0002874, originating from exon 2 of GLIS3), was validated by microarray and qRT-PCR. Functional experiments uncovered that up-regulation of circGLIS3 promoted glioma cell migration and invasion, and showed aggressive characteristics in tumor-bearing mice. Fluorescence in situ hybridization, RNA pull-down, RNA immunoprecipitation and immunohistochemical staining showed that circGLIS3 could promoted Ezrin T567 phosphorylation. Further investigation showed that circGLIS3 could be excreted by glioma through exosomes and induced endothelial cells angiogenesis. This study indicates that circGLIS3 is up-regulated in high-grade glioma and contributes to the invasion and angiogenesis of glioma via promoting Ezrin T567 phosphorylation.

2021-09-22 | GSE165859 | GEO

CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

Project description:CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

| PRJNA698359 | ENA

CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

Project description:CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

| PRJNA698582 | ENA

Ezrin knockdown in SW480

Project description:Analysis of SW480 cells following knockdown of Ezrin using RNAi. Ezrin is a protein that regulate the organization of cytoskeleton. Ezrin KD SW480 was used to study the role of ezrin in colon cancer. Keywords: ezrin, colon cancer, migration

2008-04-29 | GSE11279 | GEO

p-Ezrin (Thr567) regulates Hippo pathway and Yap in liver

Project description:It has been shown that up regulation activity of CD81(TAPA-1, the portal of entry of Hepatitis C virus) by agonistic antibody results in phosphorylation of Ezrin. We have previously shown that in liver, Ezrin phosphorylation occurs via Syk kinase, causing suppression of hippo intensity, therefore increases sequential Yap activity. The opposite occurs when Glypican-3 (GPC3) or E2 protein of HCV bind to CD81. Mice over-expressing GPC3 in hepatocytes have decreased p-Ezrin(Thr567) and Yap, increased Hippo activity and suppressed liver regeneration. The role of Ezrin in these processes has been speculated, but not proven. We now provide dynamic picture of Ezrin regulates Hippo pathway and Yap. Forced expression of plasmids expressing mutant Ezrin (T567D) (which mimics p-Ezrin(Thr567)) suppressed Hippo activity and activated Yap signaling. And this mutant Ezrin drive more cell proliferation to cell division through up regulated Yap activity in vitro and in vivo. CD81 loses expression, while p-Ezrin(Thr567) increases in JM1 and JM2 hepatocellular carcinoma (HCC) cells. Administration with compound NSC668394, a characterized p-Ezrin(Thr567) antagonist, caused significant decrease in HCC cell proliferation. We additionally present evidence that pEzrin(T567) is also controlled by EGFR and MET. Conclusions: Ezrin phosphorylation, mediated by CD81 associated Syk kinase, is directly involved in regulation of Hippo pathway, Yap levels and growth rates of normal and neoplastic hepatocytes. The finding has mechanistic and potentially therapeutic applications in understanding and regulating growth of hepatocytes and HCC and HCV pathogenesis. We used microarrays to detail the global programme of gene expression in GFP positive hepatocytes of FVB mice adminstration with EzrinT567D plasmids

2020-03-27 | GSE145572 | GEO

RNAi profiling by array of SW840 cells after Ezrin knockdown

2008-06-11 | E-GEOD-11279 | biostudies-arrayexpress

Ezrin drives adaptation of monocytes to the inflamed lung microenvironment

Project description:Ezrin, an actin-binding protein, plays a crucial role in organizing the cellular cortical cytoskeleton and plasma membrane during cell migration, adhesion, and proliferation. While there is a good understanding of ezrin's function in cell types such as epithelial cells and lymphocytes, its role in monocytes/macrophages (MΦs) is less understood. Here, we used a monocyte/MΦ-specific ezrin knock-out mouse model to investigate the contribution of ezrin to monocyte recruitment and adaptation to the lung extracellular matrix (ECM) in response to lipopolysaccharide (LPS). Our study revealed that LPS induces ezrin expression in monocytes/MΦs, and that ezrin is essential for monocytes to adhere to lung ECM, proliferate, and differentiate into tissue-resident interstitial MΦs. Notably, ezrin is not required for monocyte extravasation into the lung parenchyma. Mechanistically, the loss of ezrin in monocytes disrupts activation of FAK and AKT signaling, which are necessary for lung-recruited monocytes and monocyte-derived MΦs to adhere to the ECM, proliferate, and survive. In summary, our data suggest that ezrin plays a role beyond structural cellular support, influencing diverse monocytes/MΦ processes and signaling pathways in response to infections, driving their adaptation to the lung microenvironment.

2024-11-07 | GSE267506 | GEO

Expression data in ezrin-knockdown ec109 cells(PSE1) and control(PS)

Project description:Ezrin belongs to the ezrin¨Cradixin¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Keywords: Gene expression after RNAi

2006-11-09 | GSE6233 | GEO

siRNA profiling of human ezrin-knockdown ec109 cells(PSE1) and control(PS)

Project description:Ezrin belongs to the ezrinÂ¨CradixinÂ¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Experiment Overall Design: he mammalian expression vector, pSUPER.neo.circular (OligoEngine), was used for expression of siRNA in EC109 cells. Briefly, two primer pairs were synthesized, one pair encoding nucleotides 274Â¨C292 (TCCACTATGTGGATAATAA) followed by a 9 base Â¡Â®Â¡Â®loopÂ¡Â¯Â¡Â¯ (TTCAAGAGA) and the inverted repeat (PSE1), and the second encoding nucleotides 265Â¨C283 (ACTTTGGCCTCCACTATGT) again followed by the loop and inverted repeat (PSE2). And pSUPER.neo vector of nonspecific siRNA was taken as negative control (PSC). The primer pairs were annealed and inserted into the BglII and HindIII sites of pSUPER.neo and transformed into JM109 competent cells (Promega). Positive clones were verified and transfected into EC109 cells using FuGENE 6 transfection reagent (Roche) according to the manufacturerÂ¡Â¯s instructions. G418 (400 Â¦Ãg/ml, Calbiochem) was added into the culture medium after 24 h. Stable G418-resistant clones were obtained in 7Â¨C9 days. The expanded cells were then used for subsequent studies.

2008-06-14 | E-GEOD-6233 | biostudies-arrayexpress

Functional marker in glioblastoma

Project description:To identify receptors and pathways active in glioblastoma (GBM) stem like cells (GSCs), we generated and screened thousands of monoclonal antibodies (mAbs) for preferential binding to primary cultures enriched in GSCs. This led to the identification of the integrin alpha 7 (ITGA7) as a major laminin receptor in GSCs and in primary high-grade glioma specimens. Analyses of mRNA profiles in comprehensive datasets revealed that high ITGA7 expression was negatively correlated with survival of patients with both low- and high-grade glioma. In vitro and in vivo analyses demonstrated a key biological function of ITGA7 in growth and invasion of GSCs. In addition, we showed that targeting ITGA7 by RNAi or blocking mAbs impaired laminin-induced signaling and led to a significant delay of tumor engraftment and strong reduction in size and invasion. Our data underline the potential value of ITGA7 as glioma biomarker and therapeutic target.

2018-01-10 | PXD006069 | Pride

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