Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14302109_1.fastq.gz | Fastqsanger.gz | |||
| SRR14302109_2.fastq.gz | Fastqsanger.gz | |||
| SRR14302110_1.fastq.gz | Fastqsanger.gz | |||
| SRR14302110_2.fastq.gz | Fastqsanger.gz | |||
| SRR14302111_1.fastq.gz | Fastqsanger.gz |
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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.
2020-07-04 | GSE100775 | GEO
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.
2013-06-03 | E-GEOD-44122 | biostudies-arrayexpress
Project description:Temozolomide (TMZ) has been used for the treatment of glioblastoma (GBM) since last decade, but its treatment benefits are limited by acquired resistance, a process that remains incompletely understood. Here we report that a novel enhancer, located between the promoters of Ki67 and O6-methylguanine-DNA-methyltransferase (MGMT) genes, is activated in TMZ-resistant patient-derived xenograft (PDX) lines as well as in recurrent tumor samples. Activation of the enhancer correlates with increased MGMT expression, a major known mechanism for TMZ resistance. We show that forced activation of the enhancer in cell lines with low MGMT expression results in elevated MGMT expression. Deletion of this enhancer in cell lines with high MGMT expression leads to reduced levels of MGMT and Ki67, increased TMZ sensitivity and impaired proliferation. Together, these studies uncover a novel mechanism that regulates MGMT expression, confers TMZ resistance and potentially regulates tumor proliferation.
2018-07-13 | GSE113816 | GEO
Project description:Temozolomide (TMZ) resistance may contribute to the treatment failure in patients with glioblastoma (GBM). Hence, understanding the underlying mechanisms and developing effective strategies against TMZ resistance are highly desired in the clinic. long non-coding RNAs (lncRNAs) have emerged as new regulatory molecules with diverse functions in biological processes and been deregulated in many pathologies, involved in the therapeutic resistance. It is urgent to elucidate the underlying lncRNA-based mechanisms of TMZ resistance in GBM patients.
2019-04-12 | GSE113510 | GEO
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).
2024-02-13 | GSE253458 | GEO
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
2015-10-01 | GSE68029 | GEO
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.
2020-07-03 | GSE100736 | GEO
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
Project description:Temozolomide (TMZ) resistance of glioma cells is currently a critical problem in glioma clinical treatment. In this study, we reveal a bivalent function of a super-enhancer RNA LINC02454 in modulating glioma cell sensitivity to TMZ via regulation of SORBS2 and DDR expression. LINC02454 increased TMZ sensitivity by maintaining 3D chromatin structure and promoting SORBS2 expression, but paradoxically decreased TMZ sensitivity by binding to the DDR1 locus and promoting DDR1 transcription. This study proposes a new regulatory mechanism governing glioma cell sensitivity to TMZ and provides new insights that may improve therapies against glioma.
2024-01-10 | GSE229600 | GEO