Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect daunorubicin treatment on the transcriptome of HCT116 cells [RNA-seq]

ABSTRACT: We used RNA-seq to measure the transcriptome of HCT116 in response to the DNA damaging agent daunorubicin

ORGANISM(S): Homo sapiens

PROVIDER: GSE86190 | GEO | 2016/09/30

SECONDARY ACCESSION(S): PRJNA340780

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect daunorubicin on the binding of the cohesin subunit Rad21 in HCT116 cells [ChIP-seq]

Project description:We used ChIP-seq to measure the binding of the cohesin subunit Rad21 in response to daunorubicin treatment in HCT116 cells

2016-09-30 | GSE86191 | GEO

Effect of condensate perturbing CR3 peptide on HCT116 gene expression

Project description:To measure the effect of CR3 condensate perturbing we generated HCT116 clonal cell lines that inducibly express mCherry, mCherry-CR3, mCherry-scramble-control peptides

2023-10-11 | GSE208345 | GEO

RNA-seq analysis of dolastatin 15 treatment in HCT116 cells

Project description:Dolastatin 15 is a known tubulin binding agent and shows remarkable differential cytotoxicity against a panel of colorectal HCT116 isogenic cells. The compound causes anti-vascularization effect in human endothelial cells (HUVEC) in a dose dependent manner. Antiangiogenic effect was further validated in a zebrafish genetic model with activated HIF

2020-03-22 | GSE128748 | GEO

Selective inhibition of yeast regulons by daunorubicin

Project description:The antitumor drug daunorubicin exerts some of its cytotoxic effects by binding to DNA and inhibiting the transcription of different genes. We analysed this effect in vivo transcriptome level using the budding yeast Saccharomyces cerevisiae as a model and sublethal concentrations of the drug to minimise general toxic effects. The effects of daunorubicin treatment on the yeast transcriptome are consistent with a model in which this drug impairs binding of different transcription factors by competing for their DNA binding sequences, therefore limiting their effectiveness and affecting the corresponding regulatory networks. This proposed mechanism might have broad therapeutic implications against cancer cells growing under hypoxic conditions. Keywords: Time course experiment (treated versus non-treated)

2009-12-08 | GSE19351 | GEO

Selective inhibition of yeast regulons by daunorubicin

2010-05-18 | E-GEOD-19351 | biostudies-arrayexpress

Effect of wtp53-reactivating drug RITA on HCT116 cells

Project description:Since its discovery as a tumour suppressor some fifteen years ago, the transcription factor p53 has attracted paramount attention for its role as “the guardian of the genome”. TP53 mutations occur so frequently in cancer, regardless of patient age or tumour type, that they appear to be part of the life history of at least 50% of human tumours. In most tumours that retain wild-type p53, its function is inactivated due to deregulated HDM2, a protein which binds to p53 and which can inhibit the transcriptional activity of p53 and induce its degradation. RITA is a low-molecular-weight compound which addresses the second group of tumours retaining functionally reactive wt p53. It was found in a screening of the National Cancer Institute (NCI) library of low-molecular-weight compounds based on its ability to selectively kill wtp53-containing cells. RITA binds directly to p53 and diplaces its main destructor Mdm2, as well as inducing a shift in the conformation of p53. This is in contrast to the wtp53-reactivating compound Nutlin3a, which targets Mdm2, inhibiting its ability to degrade p53. Using microarray technology we have explored the effect of RITA on the transcriptome of isogenic cell-lines with knocked-out (KO) or intact (WT) TP53. While the effects on KO cells are below detection limit, the effects on WT cells are profound. The known p53 targets induced are predominately apoptotic, in contrast to the genes affected by Nutlin3a, which are exclusively growth-arrest genes. Keywords: Antitumor agent HCT116 parental and HCT116 p53-null (HCT116 TP53-/-) cells were subjected to treatment with 1uM RITA for 12h, or left untreated. The experiment was done in three independent biological replicates.

2009-02-28 | E-GEOD-11578 | biostudies-arrayexpress

RFX7-regulated transcriptome in HCT116

Project description:RFX7-regulated transcriptome in HCT116

| PRJNA680772 | ENA

Effect of depletion of MIB1 in HCT116 cells

Project description:To investigate gene regulation by MIB1 in HCT116 cells, we established stable knockdown HCT116 cell lines.

2022-11-22 | GSE218399 | GEO

HCT116-Clone2 cells 24 hours after XR treatment at 4 Gy

Project description:cDNA microarray study of X-radiation (XR) resistant HCT116-Clone2 cells 24 hours after XR treatment at 4Gy versus unirradiated HCT116-Clone10 cells. HCT116-Clone10 cells have similar XR response with parental HCT116 cells. Keywords = X-radiation (XR) Keywords = XR resistant Keywords = colorectal cancer cells Keywords = HCT116 Keywords: repeat sample

2004-06-04 | GSE801 | GEO

HCT116-Clone2 cells 6 hours after XR treatment at 4 Gy

Project description:cDNA microarray study of X-radiation (XR) resistant HCT116-Clone2 cells 6 hours after XR treatment at 4Gy versus unirradiated HCT116-Clone10 cells. HCT116-Clone10 cells have similar XR response with parental HCT116 cells. Keywords = X-radiation (XR) Keywords = XR resistant Keywords = colorectal cancer cells Keywords = HCT116 Keywords: repeat sample

2004-06-04 | GSE800 | GEO

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