P68 protein inhibited the growth and invasion of glioma cells by adjusting the DUSP5
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407877 | ENA |
REPOSITORIES: ENA
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Project description:Preliminary research shows that,The P68 protein was highly expressed in the glioma tissue specimen and was associated with the patient's survival.Inhibition of P68 protein expression in glioma cell lines inhibits the growth, invasion and appreciation of tumor cells.In this study, gene chip was used to search for new downstream genes DUSP5 that affect the growth of glioma.The expression of inhibition or overexpression of P68 protein in glioma cell lines was consistent with the expression of expression DUSP5 and the effect of reduction DUSP5 on the growth of the tumor.The ability of the tumor to recover after the expression of DUSP5 expression in glioma cells was reduced,This indicates that P68 regulates the growth, increment and invasion of glioma cells.Through affymetrix gene chip, we use 3 biological specimens.That is three SIP68 , control of the glioma cells that infect NC.Try to get P68 protein regulated downstream gene by knocking down P68 protein.
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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.
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Project description:Gliomas are mostly incurable secondary to their diffuse infiltrative nature. Thus, specific therapeutic targeting of invasive glioma cells is an attractive concept. As cells exit the tumor mass and infiltrate brain parenchyma, they closely interact with a changing micro-environmental landscape that sustains tumor cell invasion. In this study, we used a unique microarray profiling approach on a human glioma stem cell (GSC) xenograft model to explore gene expression changes in situ in invading glioma cells compared to tumor core, as well as changes in host cells residing within the infiltrated microenvironment relative to the unaffected cortex. Replicate sets of mice (n=4) were inoculated with either of two different GSC's derived from from human glioma, and each mouse had samples taken from the tumor mass, the infiltrating area and the mouse brain parenchyma, resulting in 3 samples per animal. The tumor mass and infiltrating samples were hybridized on human U133Plus2 Arrays, whereas the infiltrating samples and mouse brain parenchyma were hybridized on mouse
2014-02-20 | E-GEOD-53717 | biostudies-arrayexpress
Project description:Gliomas are mostly incurable secondary to their diffuse infiltrative nature. Thus, specific therapeutic targeting of invasive glioma cells is an attractive concept. As cells exit the tumor mass and infiltrate brain parenchyma, they closely interact with a changing micro-environmental landscape that sustains tumor cell invasion. In this study, we used a unique microarray profiling approach on a human glioma stem cell (GSC) xenograft model to explore gene expression changes in situ in invading glioma cells compared to tumor core, as well as changes in host cells residing within the infiltrated microenvironment relative to the unaffected cortex.
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Project description:Substantial data indicate that microRNA-21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins. This miRNA has been implicated in various aspects of carcinogenesis, including cellular proliferation, apoptosis and migration. We demonstrate that miR-21 regulates multiple genes associated with glioma cell apoptosis, migration, and invasiveness, including RECK and TIMP3, suppressors of malignancy and inhibitors of matrix metalloproteinases (MMPs). Specific inhibition of miR-21 with antisense olgonucleotides leads to elevated levels of RECK and TIMP3 and therefore reduces MMP activities in vitro and in a human model of glioma in nude mice. Moreover, down-regulation of miR-21 in glioma cells leads to decrease of their migratory and invasion abilities. Our data suggest that miR-21 contributes to the glioma malignancy by down-regulation of MMP inhibitors that leads to activation of MMPs thus promoting invasiveness of cancer cells. Our results also indicate that inhibition of a single oncomir like miR-21 with specific antisense molecules can provide a novel therapeutic approach for “physiological” modulation of multiple proteins whose expression is de-regulated in cancer.
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Project description:The paper describes a model of glioma.
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This model is described in the article:
A mathematical model of pre-diagnostic glioma growth
Marc Sturrock, Wenrui Hao, Judith Schwartzbaum, Grzegorz A. Rempala
J Theor Biol. 2015 September 7; 380: 299–308
Abstract:
Due to their location, the malignant gliomas of the brain in humans are very difficult to treat in advanced stages. Blood-based biomarkers for glioma are needed for more accurate evaluation of treatment response as well as early diagnosis. However, biomarker research in primary brain tumors is challenging given their relative rarity and genetic diversity. It is further complicated by variations in the permeability of the blood brain barrier that affects the amount of marker released into the bloodstream. Inspired by recent temporal data indicating a possible decrease in serum glucose levels in patients with gliomas yet to be diagnosed, we present an ordinary differential equation model to capture early stage glioma growth. The model contains glioma-glucose-immune interactions and poses a potential mechanism by which this glucose drop can be explained. We present numerical simulations, parameter sensitivity analysis, linear stability analysis and a numerical experiment whereby we show how a dormant glioma can become malignant.
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2024-09-02 | BIOMD0000000801 | BioModels