LncRNA and mRNA expression data from TMZ-resistant cell line
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PROVIDER: PRJNA821180 | ENA |
REPOSITORIES: ENA
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Project description:Glioblastoma multiforme (GBM) is the most common and lethal malignant primary brain tumor. Temozolomide (TMZ) is a promising chemo-therapeutic agent to treat GBM. However, resistance to TMZ develops quickly with a high frequency. The mechanisms underlying GBM cells’ resistance to TMZ are not fully understood. Long non-coding RNAs (lncRNAs) are aberrantly expressed in many cancers and are highly involved in their pathogenesis including drug-resistence. In order to systematically study the role of lncRNAs in GBM cells' resistence to TMZ , we built gene expression profiles of TMZ-resistant cell line and TMZ-sensitive cell line using lncRNA and mRNA gene expression microarrays.
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Project description:The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells and to find potential therapeutic targets of GBM for improving the survival of patients.
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Project description:Glioblastoma multiforme(GBM) is the most common and lethal malignant primary brain tumor. Temozolomide (TMZ) is a promising chemo-therapeutic agent to treat GBM. However, resistance to TMZ develops quickly with a high frequency. The mechanisms underlying GBM cells’ resistance to TMZ are not fully understood. Non-coding RNAs are aberrantly expressed in many cancers and are highly involved in their pathogenesis including drug-resistence. In order to systematically study the role of miRNAs in GBM cells' resistence to TMZ , we built gene expression profiles of TMZ-resistant cell line and TMZ-sensitive cell line using miRNA gene expression microarrays.
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Project description:Differential transcriptome analysis between control cells (U87MG), TMZ-resistant cells with continuous TMZ treatment (U87MG R50) and TMZ-resistant cells with interrupted treatment (U87MG OFF R50).
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Project description:LncRNA and mRNA expression data from TMZ-resistant cell line
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Project description:Comparison of parental GSC (GSC-parental) with treatment resistant GSC clones survived 500uM TMZ treatment (GSC-500uM TMZ) We used microarrays to identify defense profiles of GSC-500uM TMZ
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Project description:We present RNA-Seq data obtained from U251 control cells and U251 cells with stable overexpression of lncRNA XLOC13218 to identify differentially expressed genes. The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells. LncRNA XLOC013218 (XLOC) was drastically upregulated in TMZ-resistant cells and was associated with poor prognosis in glioma. Overexpression of XLOC markedly increased TMZ resistance, promoted proliferation, and inhibited apoptosis in vitro and in vivo. In addition, RNA-seq analysis and gain-of-function or loss-of-function studies revealed that PIK3R2 was the potential target of XLOC. Mechanistically, XLOC recruited Specificity Protein 1 (Sp1) transcription factor and promoted the binding of Sp1 to the promoters of PIK3R2, which elevated the expression of PIK3R2 in both mRNA and protein levels. Finally, PIK3R2-mediated activation of the PI3K/AKT signaling pathway promoted TMZ resistance and cell proliferation, but inhibited cell apoptosis. In conclusion, these data highlight the vital role of XLOC/Sp1/PIK3R2/PI3K/AKT axis in GBM TMZ resistance.
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Project description:For the comparison of 6BG/TMZ with control sample, the predominant annotation among the upregulated genes is M-bM-^@M-^XapoptosisM-bM-^@M-^Y. The majority of the downregulated genes is assigned to heat shock proteins and proteins which bind unfolded proteins. To look at early changes in gene expression, primary human myeloid precursor cells (40 x 10^6 per sample) derived from 3 pooled CD34+ products were treated for 18 hours with control (vehicle), 6BG, TMZ, or 6BG/TMZ and cell pellets flash frozen. Total RNA were isolated at Miltenyi Biotec (Cologne, Germany) and bioinformatics analysis of four microarray datasets was performed by their Bioinformatics Group. The direct comparisons were: 6BG/TMZ vs Control, TMZ vs 6BG, 6BG/TMZ vs 6BG, 6BG/TMZ vs TMZ. A two-dye competitive hybridization of mRNAs derived from differently treated human cells in comparison to a reference mRNA derived from cells which underwent a different treatment was conducted. After treatment with two different drugs or a combination of both drugs, respectively, RNA was extracted from the cells and hybridized against the corresponding reference mRNA. As microarray platform, the PIQORM-bM-^DM-" Cell Death Microarray with 494 probes was used.
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Project description:LncRNA and mRNA expression of cisplatin-resistant versus parental SCC9 cells
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