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Gene expression after treatment with Nutlin 3a (Nut) and Selinexor (Sel) in Neuroblastoma Cells

ABSTRACT: Gene expression after treatment with Nutlin 3a (Nut) and Selinexor (Sel) in Neuroblastoma Cells

PROVIDER: PRJNA565248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10108573.fastq.gz	Fastqsanger.gz
	SRR10108574.fastq.gz	Fastqsanger.gz
	SRR10108575.fastq.gz	Fastqsanger.gz
	SRR10108576.fastq.gz	Fastqsanger.gz
	SRR12979655.fastq.gz	Fastqsanger.gz

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Gene expression after treatment with Nutlin 3a (Nut) and Selinexor (Sel) in Neuroblastoma Cells

Project description:Gene expression after treatment with Nutlin 3a (Nut) and Selinexor (Sel) in Neuroblastoma Cells RNA from NBAT1 knockdown and its respective control (Csh) SH-SY5Y cells after nutlin-3a (10 uM) or DMSO treatement were isolated and sequenced using BGI DNBseq. IMR32 cells were treated with either DMSO, Nut, Sel and with both Nul and Sel and RNA was isolated following treatemnet We observed that knowndown of the NBAT1 lncRNA in NB cells leads to perturbation of the P53 mediated gene expression. Combination treatment with with Nul and Sel in IMR32 cells leads to higher P53 mediated gene expression.

2020-12-23 | GSE137366 | GEO

Expression data from human sarcoma patient samples treated with either vehicle control or Nutlin-3a

Project description:This study has examined the molecular mechanisms underlying sensitivity of sarcomas to Nutlin-3a, a non-genotoxic activator of the p53 pathway. Human patient material was collected immediately following surgical resection, dissected into small pieces and ex planted onto gelatin sponges immersed in media containing either vehicle control or Nutlin-3a (10uM and/or 50uM) for 48 hours. Nutlin-3a represents a novel targeted therapy for the treatment of sarcomas. We have examined expression profiles of genes upregulated in sarcoma patient derived tissues following nutlin-3a treatment ex vivo 16 samples ((Vehicle control and Nutlin-3a (10uM and 50uM) treated samples)) from 6 sarcoma patients

2014-03-10 | E-GEOD-48296 | biostudies-arrayexpress

ATAC-seq from Nutlin-3a-treated MCF-7 cells

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Expression data from human sarcoma patient samples treated with either vehicle control or Nutlin-3a

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Pharmacological inhibition of WIP1 sensitizes acute myeloid leukemia cells to MDM2 inhibitor Nutlin-3a

Project description:The wild-type p53-inducible protein phosphatase WIP1, encoded by the PPM1D gene, is a negative regulator of p53 and is involved in cell cycle control and DNA damage stress-response. In acute myeloid leukemia (AML), the restoration of p53 activity through MDM2 inhibition proved efficacy in a number of combination strategies. We investigated the therapeutic potential of its inhibition through the selective WIP1 inhibitor (WIP1i) GSK2830371, in association with the MDM2 inhibitor Nutlin-3a (Nut-3a) in a panel of AML cell lines and performed gene expression analysis of single agent and combined treatments. A p53-related signature was significantly upregulated in the TP53-wildtype MV-4-11 AML cell line. Moreover, drug-specific transcriptional changes likely contribute to the synergistic combination effect.

2021-05-06 | GSE156182 | GEO

Transcriptomics analysis in 3T3L1 preadipocytes with activation of p53 via Nutlin-3a treatment

Project description:3T3L1 preadipocytes were treated with DMSO control and Nutlin-3a (prepared in DMSO) and total RNA extracted from the treated cells were subjected to illumina based RNA-seq to analyze and compare transcriptome to understand gene expression regulation influenced by p53 activation via Nutlin-3a treatment.

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Nutlin-3a induced changes in the transcriptome of MCF-7 cells

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Nanopore long-read sequencing from Nutlin-3a-treated MCF-7 cells

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QuantSeq from Nutlin-3a-treated MCF-7, U2OS, and RPE-1 cells

Project description:QuantSeq from MCF-7, U2OS, and RPE-1 cells treated with Nutlin-3a or DMSO control

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Project description:Neuroblastoma accounts for 15% of cancer-related deaths in children, highlighting an unmet need for novel therapies. Selinexor is a small molecule inhibitor of XPO1 that shuffles cargo proteins with a nuclear export sequence, many of which are essential for cancer growth and cell maintenance, from the nucleus to the cytosol. We systematically tested the effect of selinexor against neuroblastoma cells in vitro and in vivo and used a proteomics screening approach to interrogate unknown mechanisms of action. We found that selinexor induces its cytotoxic effects in neuroblastoma through the nuclear accumulation of p53. By combining selinexor with an aurora kinase inhibitor, alisertib that is already in clinical use for neuroblastoma, we show that p53-mediated lethality can be further augmented supporting clinical testing of this drug combination against neuroblastoma

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