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Microarray analysis of U87 glioma cells after transient knockdown of FOXM1

ABSTRACT: FOXM1 plays a key role in M phase in normal cells and is overexpressed in human glioma. We found that FOXM1 deprivation could sensitize the glioma cells to TMZ chemotherapy. To find out the mechanistic regulation of FOXM1 in chemo-resistant genes, we used microarrays to select the potential genes regulated by FOXM1 which dominates in glioma chemo-resistance. U87 glioma cells were transiently transfected with none-target siRNA or FOXM1 siRNA. Total RNA were extracted after 48 hours and subjected to the microarray.

ORGANISM(S): Homo sapiens

SUBMITTER: zhang nu

PROVIDER: S-ECPF-GEOD-40051 | biostudies-other |

REPOSITORIES: biostudies-other

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Microarray analysis of U87 glioma cells after transient knockdown of FOXM1

Project description:FOXM1 plays a key role in M phase in normal cells and is overexpressed in human glioma. We found that FOXM1 deprivation could sensitize the glioma cells to TMZ chemotherapy. To find out the mechanistic regulation of FOXM1 in chemo-resistant genes, we used microarrays to select the potential genes regulated by FOXM1 which dominates in glioma chemo-resistance.

2012-08-11 | GSE40051 | GEO

Microarray analysis of U87 glioma cells after transient knockdown of FOXM1

2012-08-10 | E-GEOD-40051 | biostudies-arrayexpress

miRNA analysis of HBMVECs exposed or unexposed to U87 glioma cells

Project description:A key step in angiogenesis is the upregulation of growth factor receptors on endothelial cells. Here we demonstrate that a small regulatory microRNA, miR-296 has a major role in this process. Glioma cells and angiogenic growth factors elevate the level of miR-296 in primary human brain microvascular endothelial cells in culture. The miR-296 level is also elevated in primary tumor endothelial cells isolated from human brain tumors compared to normal brain endothelial cells. Growth factor-induced miR-296 contributes significantly to angiogenesis by directly targeting the hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) mRNA, leading to decreased levels of HGS and thereby reducing HGS-mediated degradation of the growth factor receptors VEGFR2 and PDGFR-β. Furthermore, inhibition of miR-296 with antagomirs reduces angiogenesis in tumor xenografts in vivo. Keywords: comparitive miRNA analysis 3 biological replicates (HBMVECs) are compared to 3 biological replicates (HBMVECs exposed to U87 glioma cells)

| S-ECPF-GEOD-13091 | biostudies-other

Metabolic impact of anti-angiogenic agents on U87 glioma cells.

Project description:BackgroundGlioma cells not only secrete high levels of vascular endothelial growth factor (VEGF) but also express VEGF receptors (VEGFR), supporting the existence of an autocrine loop. The direct impact on glioma cells metabolism of drugs targeting the VEGF pathway, such as Bevacizumab (Bev) or VEGFR Tyrosine Kinase Inhibitor (TKI), is poorly known.Material and methodsU87 cells were treated with Bev or SU1498, a selective VEGFR2 TKI. VEGFR expression was checked with FACS flow cytometry and Quantitative Real-Time PCR. VEGF secretion into the medium was assessed with an ELISA kit. Metabolomic studies on cells were performed using High Resolution Magic Angle Spinning Spectroscopy (HR-MAS).ResultsU87 cells secreted VEGF and expressed low level of VEGFR2, but no detectable VEGFR1. Exposure to SU1498, but not Bev, significantly impacted cell proliferation and apoptosis. Metabolomic studies with HR MAS showed that Bev had no significant effect on cell metabolism, while SU1498 induced a marked increase in lipids and a decrease in glycerophosphocholine. Accordingly, accumulation of lipid droplets was seen in the cytoplasm of SU1498-treated U87 cells.ConclusionAlthough both drugs target the VEGF pathway, only SU1498 showed a clear impact on cell proliferation, cell morphology and metabolism. Bevacizumab is thus less likely to modify glioma cells phenotype due to a direct therapeutic pressure on the VEGF autocrine loop. In patients treated with VEGFR TKI, monitoring lipids with magnetic resonance spectroscopic (MRS) might be a valuable marker to assess drug cytotoxicity.

| S-EPMC4055646 | biostudies-literature

Expression data from U87 glioma cells and U87-2M1 glioma cells

2012-12-31 | GSE35169 | GEO

Expression data from U87 glioma cells and U87-2M1 glioma cells

Project description:An experimental lung metastasis assay was used to derive an invasive subline of U87 that is metastatic in mice. We used microarray analyses to find out over-represented gene ontologies that can explain the observed enhanced invasiveness of U87-2M1 cells. Early passage U87-2M1 cells and parental U87 glioma cells from ATCC were selected for RNA extraction and hybridization on microarray

2012-12-31 | E-GEOD-35169 | biostudies-arrayexpress

Effects of silencing miR-10b in an U87-2M1 glioma line - an invasive in vivo derived subline of U87 glioma cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

| S-ECPF-GEOD-35208 | biostudies-other

Microarray analysis of prothrombin knockdown in zebrafish.

Project description:The serine protease thrombin is generated from its precursor, prothrombin, in the coagulation cascade and plays a central role in fibrin deposition and platelet activation mediated through the protease activated receptors. Knockdown of prothrombin in the zebrafish was previously shown to recapitulate the phenotype observed in prothrombin knockout mice, such as an absence of blood pericardial edema, and hemorrhage. However, the role of thrombin during embryogenesis is not fully understood. To find genes affected by potential thrombin signaling in embryogenesis before blood circulation, microarray analysis was performed using total RNA prepared from antisense-injected, knockdown embryos versus mismatch-injected at 20 h post fertilization. A total of 63 upregulated and downregulated genes were identified with duplicate microarrays using dye reversal and a two-fold difference limitation. Real time RT-PCR for 10 selected genes identified by the microarray confirmed the expression changes in these genes. One particular gene, phlda3, was at least eleven fold upregulated, and in situ hybridization revealed expansion of phlda3 expression in the central nervous system, branchial arches, and head endoderm in knockdown embryos. The identification of these genes regulated by thrombin according to microarray analysis should provide a greater understanding of the effects of thrombin activity in the early vertebrate embryo.

| S-EPMC2763619 | biostudies-literature

FoxM1 promotes glioma cells progression by up-regulating Anxa1 expression.

Project description:Forkhead box M1 (FoxM1) is a member of the forkhead transcription factor family and is overexpression in malignant gliomas. However, the molecular mechanisms by which FoxM1lead to glioma carcinogenesis and progression are still not well known. In the present study, we show that Anxa1 was overexpression in gliomas and predicted the poor outcome. Furthermore, Anxa1 closely related to the FoxM1 expression and was a direct transcriptional target of FoxM1. Overexpression of FoxM1 up-regulated Anxa1 expression, whereas suppression of FoxM1 expression down-regulated Anxa1 expression in glioma cells. Finally, FoxM1 enhanced the proliferation, migration, and angiogenesis in Anxa1-dependent manner both in vitro and in vivo. Our findings provide both clinical and mechanistic evidences that FoxM1 contributes to glioma development by directly up-regulating Anxa1 expression.

| S-EPMC3753245 | biostudies-literature

RNAi-mediated knockdown of VDR surprisingly suppresses cell growth in Jurkat T and U87-MG cells.

Project description:Vitamin D receptor (VDR) is a nuclear receptor for 1,25-Dihydroxyvitamin D3. VDR is expressed in many types of cells and involved in different biological processes such as immunity and inflammation. In addition, the role for VDR has been indicated in different diseases including multiple sclerosis (MS). In this study, we investigated the effects of VDR knockdown on growth, apoptosis, cell cycle, and some inflammatory gene expressions in Jurkat and U87-MG cell lines. The cell lines were transfected with plasmids encoding short hairpin RNA specific to VDR mRNA. Next, growth, apoptosis, and cell cycle were evaluated using MTT assay and annexin VDR along with flowcytometry. Then the mRNA expression of some genes was determined by real-time PCR at 24 h and 48 h after transfection. The cell growth and apoptosis of VDR-shRNA transfected Jurkat T cells and U87-MG cells were surprisingly changed compared with those in control cells. The expression of IL-10, NF-KB, TGF-β1, TGF-β R I, and TGF-β R II in two cell lines transfected with VDR-shRNA was significantly changed compared to control cells. VDR showed a new unexpected function to control cell growth in vitro. In addition, while VDR knocking down in two different cell lines of U87-MG and Jurkat cells had different effects on NF-kB and TGF-beta expression levels, its effects on cell growth and apoptosis were similar. This may suggest that these two different cell lines can show similar anti-proliferative effects by different downstream signalling pathways. Therefore, these data may be useful to design novel diagnostic and therapeutic methods for diseases such as MS.

| S-EPMC6861732 | biostudies-literature

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