Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from EGF-stimulated A431 cells with or without Gefitinib treatment

ABSTRACT: Expression data from EGF-stimulated A431 cells with or without Gefitinib treatment

PROVIDER: PRJNA641441 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Human colon cancer cell lines: NT(untreated) vs EGF, Cetuximab and Gefitinib treatments

Project description:Gene Expression Profiling of HT-29 and Caco-2 colon cancer cell lines untreated compared with EGF, Cetuximab, Gefitinib,EGF plus Cetuximab and EGF plus gefitinib treatments. Keywords: Gene Expression Profiling

2007-09-12 | GSE8967 | GEO

RNA-seq of A431 cell line after gefitinib treatment

Project description:RNA sequencing of A431 cell line samples before and after gefitinib treatment, at 0, 2, 6 and 24 hours, was performed in order to characterize the cell line's early and late response to this drug, and to compare against proteomics (mass spectrometry) characterization of the cell line using the same setup. These data were used in Branca et al., HiRIEF LC-MS enables deep proteome coverage and unbiased proteogenomics., Nat Methods. 2014 Jan;11(1):59-62 (doi: 10.1038/nmeth.2732).

2016-12-01 | E-MTAB-5285 | biostudies-arrayexpress

Time-course gene expression profiles of gefitinib-sensitive or -resistant lung adenocarcinoma cells stimulated with EGF, in the presence or absence of gefitinib, EGF receptor tyrosine kinase-specific inhibitor

Project description:Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), induces substantial clinical responses for non-small cell lung cancer (NSCLC) cells harboring EGFR activating mutations, but most of them invariably develop resistance. By generating a gefitinib resistance (PC9GR) from a human NSCLC-derived drug sensitive cell line (PC9), we studied differences of transcription dynamics between them by the aid of a computational decoupling of hidden regulatory signals from time course gene expression profiles. Given a collection of transcription factors (TFs) and their regulatory targets, the method captured temporally-synchronized shifts in evolving expression of target genes sharing each TF regulatory unit, and drew underlying regulatory signals. The analysis identified sterol regulatory element binding protein 1 (SREBP-1) as a key regulatory agent that facilitates the maintenance of drug tolerance, involving transcription controls of a G1-specific cyclin dependent kinase inhibitor whose expression was specifically elevated in PC9, but in turn, reduced in PC9GR Gefitinib-resistance cell line (PC9GR) was established derived from lung adenocarcinoma cell line PC9. PC9 cells and PC9GR cells were treated with the four different conditions, control (No treatment), EGF-treatment, gefitinib-treatment, and both gefitinib and EGF-treatment. In each condition, the gene expression was measured at 26 time points during 24 hrs.

2014-01-01 | E-GEOD-34228 | biostudies-arrayexpress

Transcription profiling by array of human wild type and gefitinib-resistant A431 cancer cells

Project description:A431 wild-type (wt) cancer cell line is sensitive to treatment with EGFR tyrosine kinase inhibitors (TKIs). By culturing it chronically under gefitinib, it eventually becomes resistant (A431_GR cell). We know of a few proteins involved in this mechanism of drug resistance, but a cDNA exprssion array would add information to other genes that might be involved in this resistance mechanism. We used microarrays to identify the differences in the global gene expression between A431_wt (wild-type) cells and A431_GR cells. Experiment Overall Design: Total RNA was isolated from parental (wild-type) and GR (gefitinib-resistant) A431 cells using TRIzol reagent (Invitrogen, Carlsbad, CA), followed by RNeasy Mini Kit column purification (Qiagen, Valencia, CA) including an in column DNAse clean-up using RNAse-free DNAse Set (Qiagen). Synthesis of cRNA target, its hybridization to Human Genome U133 Plus 2.0 microarrays and scanning of those arrays was performed using Affymetrix GeneChip products and reagents in accordance with the manufacturerâs recommendations at the Vanderbilt Microarray Shared Resource.

2008-04-06 | E-GEOD-10696 | biostudies-arrayexpress

Expression data from EGF-stimulated A431 cells with or without Gefitinib treatment

Project description:Signals are transduced through multiple pathways, but it is difficult to check which pathways are responsible for each defined signal. We used microarray to examine that the signal reached at the nucleus through pathways downstream EGFR.

2020-06-24 | GSE153114 | GEO

RNA-seq of A431 cell line after gefitinib treatment

Project description:RNA-seq of A431 cell line after gefitinib treatment

| PRJEB18261 | ENA

Proximity biotinylation of A431 cells by EGFR-FabID

Project description:A431 cells were pretreated with DMSO or gefitinib and unstimulated or stimulated with EGF. Then AGIA-FabID or EGFR-FabID were added to the cells in three biological replicates. Cell lysates were subjected to methanol-chloroform precipitation and digested with trypsin. Biotinylated peptides were purified by Tamavidin 2-REV and identified by LC-MS/MS analysis.

2023-11-14 | PXD039450 | JPOST Repository

OxRAC Analysis of Cysteine Oxidation After EGF stimulation in A431 Cells

Project description:Analysis of cysteine redox networks 0, 2, 5, 15, 30, and 60 minutes after stimulation with EGF in A431 cells using a new workflow 'OxRAC' optimized to assess dynamic redox regulation.

2020-01-10 | PXD010880 | Pride

Transcription profiling of Human Endometrial Cancer Cells treated with EGF or gefitinib to investigate gene regulation of EGFR Isoforms.

Project description:Microarrays were used to analyze differential gene expression and to help determine the efficacy of Iressa (gefitinib), a tyrosine kinase inhibitor, on endometrial cancer cells. Type I Ishikawa H and type II Hec50co endometrial carcinoma cells both express EGFR and sEGFR, but differ markedly in their responsiveness to the EGFR inhibitor gefitinib. This difference is paralleled by differences in the expression of sEGFR and EGFR, as well as in their transcriptional response following treatment with either EGFor gefitinib. The small cluster of differently regulated genes reported here in these type I vs. type II endometrial cancer-derived cell lines may identify candidate biomarkers useful for predicting sensitivity to EGFR blockade. Type I (Ishikawa H cells) and type II (Hec50co) derived endometrial carcinomas, were dosed with either EGF(epidermal growth factor) or Iressa (gefitinib) for 12 or 24 hours and gene expression was examined.

2010-03-23 | E-GEOD-20854 | biostudies-arrayexpress

2014-01-01 | GSE34228 | GEO

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