Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Transcriptome changes following treatment of human cancer cells with actinomycin D, nutlin-3a or camptothecin

PROVIDER: PRJNA831359 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18961101.fastq.gz	Fastqsanger.gz
	SRR18961102.fastq.gz	Fastqsanger.gz
	SRR18961103.fastq.gz	Fastqsanger.gz
	SRR18961104.fastq.gz	Fastqsanger.gz
	SRR18961105.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Transcriptomic and proteomic study of cancer cell lines exposed to actinomycin D and nutlin-3a reveals numerous, novel candidates for p53-regulated genes

Project description:Transcriptomic analyses revealed hundreds of p53-regulated genes, however these studies used a limited number of cell lines and p53-activating agents. Therefore, we searched for candidate p53-target genes by employing stress factors and cell lines never used in high-throughput search for p53-regulated genes. We performed RNA-Seq on A549 cells exposed either to camptothecin, actinomycin D, nutlin-3a or to a combination of actinomycin D and nutlin-3a (A+N). The latter two substances synergize in activation of selected p53-target genes. Similar analysis was performed on other cell lines (U-2 OS, NCI-H460, A375) exposed to A+N. Mass spectrometry was employed to identify proteins in cell lysates or those secreted to the medium of A549 cells in control conditions or treated with A+N. Expression of selected genes strongly upregulated by A+N or camptothecin was examined by RT-PCR in p53-deficient cells and their controls. We found that p53 participates in upregulation of: ACP5, APOL3, CDH3, CIBAR2, CRABP2, CTHRC1, CTSH, FAM13C, FBXO2, FRMD8, FRZB, GAST, ICOSLG, KANK3, KCNK6, KLRG2, MAFB, MR1, NDRG4, PTAFR, RETSAT, TMEM52, TNFRSF14, TRANK1, TYSND1, WFDC2, WFDC5, WNT4 genes. Twelve of their proteins were detected in the secretome and/or proteome of treated cells. Our data generate new hypotheses concerning functioning of p53 tumor suppressor.

2026-05-31 | PXD036860 | Pride

Project description:Transcriptome changes following treatment with actinomycin D and nutlin-3a and/or CHIR-98014

| PRJNA757776 | ENA

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

2014-03-10 | GSE48296 | GEO

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

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

Project description:Transcriptome changes following treatment of three human cancer cell lines (U-2 OS, NCI-H460, A375) with actinomycin D and nutlin-3a.

| PRJNA837373 | ENA

PolyA RNA-seq from CHP212 WT and FAM193AKO cells treated with Nutlin-3

Project description:Analysis of steady-state mRNA levels in CHP212 WT and FAM193AKO cells following DMSO or Nutlin-3a treatment.

2022-12-19 | GSE189133 | GEO

Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) of BJ cells treated with Nutlin-3a, an MDM2 inhibitor, which induces p53.

Project description:We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells in which p53 was induced by Nutlin-3a RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs Ribosome profiling was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs

2013-06-01 | E-GEOD-45785 | biostudies-arrayexpress

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

p53-dependent transcription in hTERT-RPE1 cells

Project description:We investigated the genes that were most strongly activated by p53 in this immortalized human cell line following treatment with the MDM2 inhibitor nutlin-3a. To identify genes that were activated by p53, we comparatively analyzed parental cells and isogenic derivatives. Wild type, p53-knockout and cells harboring a heterozygous p53 A276P mutation were assessed.

2023-05-01 | GSE229160 | GEO

Expression data from polarized macrophages: effect of p53

Project description:p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease. We used microarrays to study the global programme of gene expression in nutlin-3a and 10058F4 (C-myc inhibitor) treated polarised mouse macrophages 5 groups of cultured mouse macrophages: (i) M0 (untreated), (ii) M1, (iii) M2, (iv) M2+nutlin-3a, (v) M2+MYC inhibitor (10058F4). 3 biological replicates per treatment group.

2015-01-01 | E-GEOD-53321 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data