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Influence of evernic acid alone and in combination with temozolomide on gene expression of U-87 glioblastoma cell line

ABSTRACT: Influence of evernic acid alone and in combination with temozolomide on gene expression of U-87 glioblastoma cell line

PROVIDER: PRJNA1030383 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26453042.fastq.gz	Fastqsanger.gz
	SRR26453043.fastq.gz	Fastqsanger.gz
	SRR26453044.fastq.gz	Fastqsanger.gz
	SRR26453045.fastq.gz	Fastqsanger.gz
	SRR26453046.fastq.gz	Fastqsanger.gz

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Influence of evernic acid alone and in combination with temozolomide on gene expression of U-87 glioblastoma cell line

Project description:to investigate the sensitization mechanism of temozolomide-resistant U-87 cells by evernic acid, we established gene expression of U-87 cells treated with evernic acid, temozolomide and their combinations compared to the gene expression of untreated cells. The NGS-core facility of the University Hospital Bonn of Bonn University performed the RNA-sequencing.

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Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.

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RNASeq analysis of NB1691 neuroblastoma cells treated with MDM2-p53 inhibitor RG7388 alone and in combination with temozolomide

Project description:To further identify potential mechanisms involved in combining RG7388 with temozolomide, GSEA was performed and revealed that RG7388 and temozolomide act cooperatively to upregulate the p53 pathway and downregulate MYC targets, the former resulting in significantly greater induction of several apoptotic genes.

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Expression data from U-87 human glioma cells with proficient and deficient NF-кB after treatment with temozolomide

Project description:The transcription factor, NF-кB, plays a central role in the response to DNA damage. This ubiquitous family of proteins is made up of five subunits: p50 (NF-κB1, p105), p52 (NF-κB2, p100), p65 (relA), relB, and crel that appear in their mature form as dimers. Following stimulation, NF-κB dimers translocate to the nucleus where they bind specific consensus elements (κB-sites) in the promoter region of genes involved in cell survival, inflammation and the immune system. While there is a general propensity of NF-кB to mediate survival, this is not always the case and several reports note the pro-apoptotic nature of the NF-кB pathway. In examining the NF-кB response to DNA damage, we have found that the p50 subunit plays a central role in modulating cytotoxicity following TMZ treatment in malignant glioma. In the current study, given the importance of p50 to the cytotoxic response to TMZ, we set out to identify NF-кB-dependent factors that modulate the response to TMZ. U-87 glioma cells stably transfected with either control-shRNA or p105-shRNA and subsequently treated with temozolomide (TMZ) were selected for RNA extraction and hybridization on Affymetrix microarrays. Each category contains 3 biologic replicates.

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