Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from glioma cells exposed to interferon (IFN)-beta

ABSTRACT: Glioma cells are sensitized to the alkylator temozolomide after exposure to IFN-beta. In glioma-initiating cells (GIC), IFN-beta alone reduces clonogenicity. We investigated differentially expressed genes with or without IFN exposure in either longterm glioma cells or GIC. We used microarrays to investigate differential gene regulation in glioma cells after exposure to either ddH20 or IFN-beta 300 IU/ml at 6 h or 24 h.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53213 | GEO | 2014/03/31

SECONDARY ACCESSION(S): PRJNA231124

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from glioma cells exposed to interferon (IFN)-beta

Project description:Glioma cells are sensitized to the alkylator temozolomide after exposure to IFN-beta. In glioma-initiating cells (GIC), IFN-beta alone reduces clonogenicity. We investigated differentially expressed genes with or without IFN exposure in either longterm glioma cells or GIC. We used microarrays to investigate differential gene regulation in glioma cells after exposure to either ddH20 or IFN-beta 300 IU/ml at 6 h or 24 h. We used either the longterm cell line LNT-229 or the GIC cell lines GS-2 and GS-9 and exposed them to either IFN-beta 300 IU/ml or ddH20 for 6 h or 24 h.

2014-03-31 | E-GEOD-53213 | biostudies-arrayexpress

Transcription profiling of human thyroid cells exposed to INF-gamma and IL1-beta

Project description:Normal primary thyroid cells were incubated with , 100 IU/ml IFN-gamma, 50 IU/ml IL1-beta, or a combination of both IFN-gamma and IL1-beta for 24 or 72 hours. The experiment was repeated 5 times using thyroid cells from 5 different patients. RNA expression was analyzed using Affymetrix HG_U133A arrays for 3 of the thyroids, and HG_U133A_2.0 (small version of HG_U133A) arrays for 2 of the thyroids. Experiment Overall Design: Normal primary thyroid cells were incubated with , 100 IU/ml IFN-gamma, 50 IU/ml IL1-beta, or a combination of both IFN-gamma and IL1-beta for 24 or 72 hours. The experiment was repeated 5 times using thyroid cells from 5 different patients. One array was hybridized per sample (20 samples). Experiment Overall Design: The probe-set intensities with accompanying statistical analysis (2-way ANOVA) and the associated README file are included as Supplementary files.

2008-11-06 | E-GEOD-5054 | biostudies-arrayexpress

Microarray profiling analysis of lncRNAs expression in glioma cells

Project description:Tremendous studies have found that the abnormality of long noncoding RNA (lncRNA) contributed to cancer initiation, progression, and recurrence via multiple signaling cascades. Nevertheless, the possible underlying mechanisms of lncRNA in temozolomide (TMZ)-resistant glioma were not well understood, hindering the improvement of TMZ-based therapies against glioma. The present study illustrated that the lncRNA KCNQ1OT1 increased in TMZ-resistant gliomas cells compared to the parental cells. Introduction of KCNQ1OT1 boosted glioma cell viability, clonogenicity and rhodamine 123 efflux while hampered apoptosis post-exposure to TMZ. Consistent with bioinformatic prediction, KCNQ1OT1 directly sponged miR-761, which was downregulated in TMZ-resistant glioma cell lines. Overexpression of miR-761 attenuated glioma cell viability and clonogenicity while triggered apoptosis and rhodamine 123 cellular accumulation post-exposure to TMZ, leading to rehabilitated glioma TMZ-sensitivity, which was against the function of KCNQ1OT1. miR-761 bound to 3’-untranslated region of PIM1, a proto-oncogene with constitutive serine/threonine kinase activity, attenuated PIM1-mediated signaling cascades. Furthermore, stable knockdown of KCNQ1OT1 by small hairpin RNA amplified the TMZ-induced tumor regression in TMZ-resistant U251 mouse models. Briefly, the present study evaluated KCNQ1OT1 conferred TMZ resistance by sponging miR-761 and releasing PIM1 expression, resulting in activation of PIM-mediated MDR1/c-Myc/Survivin signaling pathways. The findings mentioned above extended the knowledge of lnRNA KCNQ1OT1 in the regulation of chemoresistance in glioma and provided a promising therapeutic target for TMZ-resistant glioma patients. Long noncoding RNA profiling by array

2020-10-13 | GSE144784 | GEO

Effect of INF-gamma and IL1-beta on thyroid cells

Project description:Normal primary thyroid cells were incubated with vehicle, 100 IU/ml IFN-gamma, 50 IU/ml IL1-beta, or a combination of both IFN-gamma and IL1-beta for 24 or 72 hours. The experiment was repeated 5 times using thyroid cells from 5 different patients. RNA expression was analyzed using Affymetrix HG_U133A arrays for 3 of the thyroids, and HG_U133A_2.0 (small version of HG_U133A) arrays for 2 of the thyroids. Keywords: cytokine treatments

2007-08-24 | GSE5054 | GEO

Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions

Project description:Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation. Upon the serum stimulation, the GIC spheres showed increased cellular proliferation, motility, filopodia/lameripodia formation and adhesion to the culture dishes. Simultaneously, the NSC marker proteins such as CD133 and Sox2 were down-regulated, and the astrocyte/glioma marker GFAP and the malignancy marker CD44 dramatically up-regulated. To identify genes/proteins whose expression changes dynamically during the differentiation of GICs into glioma cells, these GICs were subjected to DNA microarray/iTRAQ based integrated proteomics. Within 4 hours of tumor removal from GBM patients, tissues were subjected to GIC preparation. After successive cloning, total RNA from GIC clones (GIC03A and GIC03U) on day 2 or 7 of subculture in NSC medium with or without 10% FCS was subjected to the analysis with Affymetrix microarrays. Simultaneously, the proteins extracted from the same set of cells were subjected to LC-shot gun analyses using the 8-plex iTRAQ method. We sought to obtain the information of the common molecules that were up- or down-regulated during the GSC differentiation process, and functional targets for the early onset of GIC-associated glioma.

2013-01-26 | E-GEOD-43762 | biostudies-arrayexpress

Expression profiling of sox11-expressing glioma-initiating cell-like cells

Project description:To identify factors involved in tumorigenicity of glioma-initiating cells (GICs), we compared gene expression in GIC-like cells with and without sox11 expression. We established sox11-expressing mouse glioma-initiating cell (GIC)-like cell line (NSCL61s), NSCL61s-sox11, which lost tumorigenicity when transplanted in vivo. We think that genes, which are differently expressed between NSCL61s and NSCL61s-sox11, would be new targets for glioma therapy.

2009-11-30 | E-GEOD-17076 | biostudies-arrayexpress

Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions

2013-01-26 | GSE43762 | GEO

Gene expression in melanoma cells following treatment with IFN-beta

Project description:To further determine the candidate genes which expressed in four melanoma cells and melanocyte after treatment with IFN-β, total RNA was extracted from melanoma cells, which have different sensitivities to IFN-β, and melanocyte after treatment with or without IFN-β at a concentration of 1,000 IU/ml for 48 h. For expression profiling, oligonucleotide microarray analysis was performed at Hokkaido System Science (Sapporo, Japan) using an Agilent Human Genomic microarray 8 × 60 K version 2.0 (Agilent Technologies, Santa Clara, CA). Then, we focused on two candidate genes, CXCL-10 and IL-24, which are associated with the sensistibity of melanoma cells to IFN-β. We examined whether CXCL10 and IL-24 directly or indirectly cause sensitivitiy of melanoma to IFN-β.

2019-01-08 | GSE124759 | GEO

Expression profiles of mouse glioma-initiating cells.

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expressions between GIC-like cells and non-GICs.

2011-06-01 | GSE28091 | GEO

Expression profiling of mouse glioma-initiating cell-like cells (GICs) and non-GICs

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expression between GIC-like cells and non-GICs.

2009-12-01 | GSE17062 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data