Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281444 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The formation of U87 tumor spheres was associated with expression changes of many genes which was reverted by the treatment with ITE(2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester). We used DNA microarrays to profile gene expression in U87 tumor spheres treated with ITE and identified distinct classes of up-regulated and down-regulated genes during this process. U87 cells were selected for RNA extraction and hybridization on Affymetrix microarrays. We compared the expression profiles of parental U87 cells, U87 tumor sphere cells treated with vehicle (DMSO) and U87 tumor sphere cells treated with ITE.
2015-04-18 | E-GEOD-67986 | biostudies-arrayexpress
Project description:The formation of U87 tumor spheres was associated with expression changes of many genes which was reverted by the treatment with ITE(2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester). We used DNA microarrays to profile gene expression in U87 tumor spheres treated with ITE and identified distinct classes of up-regulated and down-regulated genes during this process.
2015-04-18 | GSE67986 | GEO
Project description:In a Kras-driven mouse model of multistage pancreatic cancer progression, decreased p-ERK levels correlate with tumor initiation. In cells derived from this model, transformed cells with low p-ERK levels express markers of pluripotency and demonstrate phenotypes of tumor initiating cells, such as formation of free-floating tumor spheres. Here, a comparison of gene expression from the 1499 cell line, which are premalignant cells isolated from mouse ADM (acinar-to-ductal metaplasia) and PanIN1 (pancreatic intraepithelial lesions), and the AH375 cell line, established from mouse PDAC, was performed.
2016-05-10 | GSE57566 | GEO
Project description:As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array. To accomplish this, mRNA expression levels of these genes were measured in the glioblastoma cell lines, U87 and U178, engineered with EGFR by retrovirus transduction (termed U87-EGFR and U178-EGFR respectively), with or without 20 ng/mL EGF treatment for 3 h. U87 and U178 cells engineered to express EGFR were stimulated with or without EGF. The experiment was replicated twice for each U87 and U178 cells.
2011-11-05 | E-GEOD-33442 | biostudies-arrayexpress
Project description:Bevacizumab induces glioblastoma resistance in two in vivo xenograft models. Two cell lines were developed with acquired resistance to bevacizumab. Gene expression difference were analyzed between treated and untreated tumors. Purpose: Antiangiogenic therapy reduces vascular permeability and delays progression but may ultimately promote an aggressive treatment-resistant phenotype. The aim of the present study was to identify mechanisms responsible for glioblastoma resistance to antiangiogenic therapy. Experimental Design: Glioma stem cell (GSC) NSC11 and U87 cell lines with acquired resistance to bevacizumab were developed from orthotopic xenografts in nude mice treated with bevacizumab. Genome-wide analyses were used to identify changes in tumor subtype and specific factors associated with resistance. Results: Mice with established parental NSC11 and U87 cells responded to bevacizumab, whereas glioma cell lines derived at the time of acquired resistance to anti-VEGF therapy were resistant to bevacizumab and did not have prolongation of survival compared to untreated controls. Gene expression profiling comparing anti-VEGF therapy-resistant cell lines to untreated controls demonstrated an increase in genes associated with a mesenchymal origin, cellular migration/invasion, and inflammation. Gene Set Enrichment Analysis (GSEA) demonstrated that bevacizumab-treated tumors showed a highly significant correlation to published mesenchymal gene signatures. Mice bearing resistant tumors showed significantly greater infiltration of myeloid cells in NSC11 and U87 resistant tumors. Invasion-related genes were also upregulated in both NSC11 and U87 resistant cells, which had higher invasion rates in vitro compared with their respective parental cell lines. Conclusions: Our studies identify multiple pro-inflammatory factors associated with resistance and identify a proneural-to-mesenchymal transition (PMT) in tumors resistant to antiangiogenic therapy. Glioma cell lines were injected into the caudate of nude mice and were allowed to grow untreated (samples labeled control) or were treated with 10 mg/kg IP twice weekly with bevacizumab (samples labeled Avastin). At the time of animal death, tumor tissue from the mouse was removed, and RNA was isolated and analyzed using gene expression. U87R and NSC11R represent cells resistant to bevacizumab (Avastin).
2013-07-01 | E-GEOD-45161 | biostudies-arrayexpress
Project description:Bevacizumab induces glioblastoma resistance in two in vivo xenograft models. Two cell lines were developed with acquired resistance to bevacizumab. Gene expression difference were analyzed between treated and untreated tumors. Purpose: Antiangiogenic therapy reduces vascular permeability and delays progression but may ultimately promote an aggressive treatment-resistant phenotype. The aim of the present study was to identify mechanisms responsible for glioblastoma resistance to antiangiogenic therapy. Experimental Design: Glioma stem cell (GSC) NSC11 and U87 cell lines with acquired resistance to bevacizumab were developed from orthotopic xenografts in nude mice treated with bevacizumab. Genome-wide analyses were used to identify changes in tumor subtype and specific factors associated with resistance. Results: Mice with established parental NSC11 and U87 cells responded to bevacizumab, whereas glioma cell lines derived at the time of acquired resistance to anti-VEGF therapy were resistant to bevacizumab and did not have prolongation of survival compared to untreated controls. Gene expression profiling comparing anti-VEGF therapy-resistant cell lines to untreated controls demonstrated an increase in genes associated with a mesenchymal origin, cellular migration/invasion, and inflammation. Gene Set Enrichment Analysis (GSEA) demonstrated that bevacizumab-treated tumors showed a highly significant correlation to published mesenchymal gene signatures. Mice bearing resistant tumors showed significantly greater infiltration of myeloid cells in NSC11 and U87 resistant tumors. Invasion-related genes were also upregulated in both NSC11 and U87 resistant cells, which had higher invasion rates in vitro compared with their respective parental cell lines. Conclusions: Our studies identify multiple pro-inflammatory factors associated with resistance and identify a proneural-to-mesenchymal transition (PMT) in tumors resistant to antiangiogenic therapy.
2013-07-01 | GSE45161 | GEO
Project description:SNAIL, which is a key factor in EMT, has high expression levels in the gastric spheres. To investigate SNAIL-regulated genes, we knocked down this gene in the gastric cancer cell line HGC-27 and compared the gene expression of these cells with those of the parental cells by microarray.
2020-02-25 | GSE145867 | GEO
Project description:mouse 4T1 breast cancer stem cell spheres were co-culutred with in vivo tumor antigen primed splenocytes, with in vivo tumor antigen primed splenocytes plus ex vivo reinforced activation via anti-CD3/CD28 beads or without co-culturing with splenocytes. Stem cell spheres were then collected and sunjected for gene expression analyses using RNA sequencing.
2022-04-06 | GSE199983 | GEO
Project description:In this project, we generated chronic sunitinib-treated 786-O cell, a renal cell carcinoma cell line. In order to investigate the possible effect of GPR30 agonist, G-1, on the growth-inhibtion related signaling pathways, we treated either parental both parental and chronic sunitinib-treated 786-O cells were treated either by vehicle-only (i.e. 0.1% DMSO) or 2 μM G-1 for 48 h. Therefore, there were three groups for comparison, including G-1 treatment (G-1 vs. parental), chronic sunitinib-treatment (SunR vs. parental), and G-1 treatment in SunR cells (SunR&G-1 vs. parental).
2021-08-14 | PXD020904 | JPOST Repository
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