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RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 72h

ABSTRACT: RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 72h

PROVIDER: PRJNA786831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17155471.fastq.gz	Fastqsanger.gz
	SRR17155472.fastq.gz	Fastqsanger.gz
	SRR17155473.fastq.gz	Fastqsanger.gz
	SRR17155474.fastq.gz	Fastqsanger.gz
	SRR17155475.fastq.gz	Fastqsanger.gz

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RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 72h

Project description:CD4 T cells from 4 healthy women were activated with aCD3 and treated with the survivin inhibitor YM155, 10 ng/ml or control during 72 hours. The last 2 hours with upplement of IFNg. The objective was to understand the action of survivin (coded by BIRC5 gene) in CD4 T cells.

2022-11-29 | GSE190351 | GEO

RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 24h

Project description:CD4 T cells from 4 healthy women were activated with aCD3 and treated with the survivin inhibitor YM155, 10 ng/ml or control during 24 hours. The last 2 hours with upplement of IFNg. The objective was to understand the action of survivin (coded by BIRC5 gene) in CD4 T cells.

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RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 24h

Project description:RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 24h

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Drug-induced mitochondrial oxidative stress is responsible for various effects of the survivin inhibitor Sepantronium Bromide (YM155) in triple negative breast cancer cells

Project description:Sepantronium bromide (YM155), a transcriptional inhibitor of anti-apoptotic protein survivin, is considered as a potential drug candidate for triple negative breast cancers (TNBC). Regardless of its excellent performance in pre-clinical models of TNBC, in patients, this drug was unable to outperform the standard chemotherapy docetaxel. The goal of this study was to identify the pathways/molecules affected by YM155 in TNBC cell lines. Detailed biochemical analysis of the paired YM155-sensitive and resistant cell lines indicates that induction of mitochondrial oxidative stress is a first-line response to the drug, ultimately leading to growth inhibition and induction of cell death. Multiple pathways involved in dampening oxidative stress-induced damages are differentially regulated in YM155-resistant cells. Furthermore, the emergence of YM155 resistance is associated with an extensive transcriptional reprogramming and alteration of many more biological pathways in addition to those identified by biochemical assays. Molecules associated with these biological pathways will potentially serve as biomarkers predicting YM155 sensitivity in TNBC cells.

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YM155 in combination with EZH2 inhibiton induces synthetic lethality

Project description:EZH2 inhibitors have been developed to treat certain cancers. To maximize the anticancer acttivity of EZH2 inhibition, we combined an EZH2 inhibitor EPZ6438 with YM155, which leads to dramatic cell death. We used microarrays to detail the global gene expression profiles.

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Single cell RNAseq at 48h and 72h in mice

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Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin. KYSE410 cell line were treated with 20 nM YM155 for 6 hrs and selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to gene expression profiles of KYSE 410 cell line treated with cisplatin.

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