Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

11 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

ABSTRACT: Potential vorinostat-resistance candidate genes were identified using RNA interference screening in vorinostat-resistant HCT116 cells (HCT116-VR) using a synthetic lethal approach. In order to understand the mechanisms by which these genes contributed to vorinostat response, transcriptomic analysis was conducted on HCT116-VR cells and those with siRNA-mediated knockdown of each of the vorinostat resistance candidate genes. There are 45 samples in total, from triplicate independent biological experiments of 15 samples each. The negative control to which all gene knockdowns are compared is the mock transfection control (mock).

ORGANISM(S): Homo sapiens

SUBMITTER: Katrina Falkenberg

PROVIDER: E-GEOD-56788 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of GLI1 or PSMD13 with or without vorinostat treatment

Project description:Transcriptome analysis was conducted on vorinostat resistant HCT116 cells (HCT116-VR) upon knockdown of potential vorinostat resistance candidate genes in the presence and absence of vorinostat. Potential vorinostat resistance candidate genes chosen for this study were GLI1 and PSMD13, which were identified through a genome-wide synthetic lethal RNA interference screen. To understand the transcriptional events underpinning the effect of GLI1 and PSMD13 knockdown (sensitisation to vorinostat-induced apoptosis), cells were first subjected to gene knockdown, then to treatment with vorinsotat or the solvent control. Two timepoints for drug treatment were assessed: a timepoint before induction of apoptosis (4hrs for siGLI1 and 8hrs for siPSMD13) and a timepoint when apoptosis could be detected (8hrs for siGLI1 and 12hrs for siPSMD13). There are 42 samples in total, from triplicate independent biological experiments of 14 samples each.

2016-06-30 | E-GEOD-57871 | biostudies-arrayexpress

RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

Project description:Potential vorinostat-resistance candidate genes were identified using RNA interference screening in vorinostat-resistant HCT116 cells (HCT116-VR) using a synthetic lethal approach. In order to understand the mechanisms by which these genes contributed to vorinostat response, transcriptomic analysis was conducted on HCT116-VR cells and those with siRNA-mediated knockdown of each of the vorinostat resistance candidate genes.

2014-07-07 | GSE56788 | GEO

RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of GLI1 or PSMD13 with or without vorinostat treatment

2016-06-30 | GSE57871 | GEO

The Pelvic Radiation and Vorinostat (PRAVO) Study - Histone Deacetylase Inhibitor Activity

Project description:The study objective was to propose molecular mechanisms of action of the histone deacetylase inhibitor vorinostat. In the PRAVO phase 1 study, patients that were scheduled to receive pelvic palliative radiation to 30 Gy in 3-Gy fractions for gastrointestinal carcinoma, were enrolled onto four sequential dose levels of vorinostat, starting at 100 mg daily with dose escalation in increments of 100 mg. Endpoints included treatment safety and tolerability, tumor response, and biological activity of vorinostat. For the purpose of identifying biomarkers of vorinostat action, peripheral blood mononuclear cells, representing normal tissue exposed to vorinostat, were used. The samples were collected, one at baseline and two on-treatment samples. The time points for sample collection were chosen based on our previous data from experimental colorectal carcinoma models exposed to vorinostat, demonstrating that the maximum tumor histone acetylation 2-3 hours after drug exposure was restored to baseline after 24 hours. In PRAVO study patients, tumor histone hyperacetylation was observed 3 hours after vorinostat administration. From the 17 patients enrolled onto the PRAVO study, a full set of three samples was obtained from 14 individuals: one baseline sample collected prior to commencement of vorinostat treatment (T0), and two on-treatment samples collected 2 and 24 hours after the patient had received the preceding daily dose of vorinostat (T2 and T24). Individual vorinostat dose levels were 100 mg (D100), 200 mg (D200), 300 mg (D300), or 400 mg (D400).

2013-05-08 | E-GEOD-46703 | biostudies-arrayexpress

The Pelvic Radiation and Vorinostat (PRAVO) Study - Histone Deacetylase Inhibitor Activity

2013-05-08 | GSE46703 | GEO

Requirement for the Mediator kinase module for activation of super-enhancer associated genes in colon cancer cells

Project description:RNA sequencing of HCT116 colon cancer cells following single and combined depletions of Mediator kinase module subunits CDK8, CDK19, MED12, MED13 and MED13L and the BET family protein BRD4. The results provide insight into the shared and specific functions of kinase module subunits and BRD4 in regulation of expression of transcriptional programs including genes associated with cancer acquired super-enhancers.

2018-04-02 | E-MTAB-5873 | biostudies-arrayexpress

Transcriptome analysis for vorinostat-treated choriocarcinoma cells

Project description:Choriocarcinoma is one of the rare gynecological malignancies with aggressive behavior. Vorinostat is an approved HDAC inhibitor, and HDACs play important roles in regulating gene expression and modulating various cellular processes. Here, the human choriocarcinoma cell lines (JAR and JEG-3) were treated with 1 μM vorinostat or DMSO for 48 h. Then, total RNA was extracted, and transcriptome analysis was performed.

2021-12-25 | GSE192446 | GEO

Vorinostat treatment of PPS-ICBR cells

Project description:We generated immune checkpoint blockade resistant cell lines from a prostate tumor driven by Probasin-Cre Pten/P53/Smad4 loxp deletion, through serial implantation and ICB treatment. We then wanted to explore whether gene expression changes associated with resistance to immune checkpoint blockade could be reversed by treating ICB resistant cells with the pan-HDAC inhibitor Vorinostat. We used a microarray to determine gene expression changes caused by Vorinostat treatment in these cells with biological duplicates.

2024-02-13 | GSE205469 | GEO

E-GEOD-56788

Project description:RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

2019-05-14 | E-GEOD-56788 | ExpressionAtlas

Homo sapiens

Project description:RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

| PRJNA244587 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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