Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from mRNA in complex with EGFR from irradiated human A549 (ATCC CCL185) cells

ABSTRACT: Immunoprecipitation of EGFR from irradiated A549 (ATCC CCL185) cells was performed in order to characterize bound mRNA species with the help of microarray analysis As control experiment, immunoprecipitation was also performed with IgG

ORGANISM(S): Homo sapiens

PROVIDER: GSE92428 | GEO | 2017/12/21

SECONDARY ACCESSION(S): PRJNA357552

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-sequencing in irradiated and normal A549 cells.

Project description:The aim of this study is to investigate the role of circRNAs/miRNAs/lncRNAs in radioresistance in A549 cells. For irradiation, A549 cells were exposed to a single fraction 2 GY or 4GY X-ray dose using an X-RAD 160-225 instrument (Precision X-Ray, Inc., Branford, CT, USA; filter: 2 mm AI; 42 cm, 225 kV/s, 12.4 mA, 2.0 Gy/min). The irradiated A549 cells (after a single dose of irradiation) and normal A549 cells were cultured for further 48h and then collected its total RNA for high-throughput sequencing.

2018-12-27 | GSE124396 | GEO

RNA-sequencing in irradiated and normal A549 cells.

Project description:RNA-sequencing in irradiated and normal A549 cells.

| PRJNA511903 | ENA

RNA-seq analysis using A549 cells with FXR knockdown and control A549 cells with or without ionizing radiation treatment.

Project description:In this study, we explored the role of FXR in the response to ionizing radiation (IR) in A549 human lung cancer cells. FXR was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), FXR knockdown A549 cells (non-irradiated), and FXR knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with FXR knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which FXR influences the cellular response to radiation and its potential impact on cancer therapy.

2024-10-31 | GSE278872 | GEO

RNA-seq analysis using A549 cells with TRIM22 knockdown and control A549 cells with or without ionizing radiation treatment.

Project description:In this study, we explored the role of TRIM22 in the response to ionizing radiation (IR) in A549 human lung cancer cells. TRIM22 was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), TRIM22 knockdown A549 cells (non-irradiated), and TRIM22 knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with TRIM22 knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which TRIM22 influences the cellular response to radiation and its potential impact on cancer therapy.

2025-01-01 | GSE277805 | GEO

miRNA expression profiling of gamma-irradiated A549 cells at 4 h after irradiation

Project description:miRNA expression profiling of gamma-irradiated A549 cells at 4 h after irradiation

| PRJNA445848 | ENA

miRNA expression profiling of gamma-irradiated A549 cells at 24 h after irradiation.

Project description:miRNA expression profiling of gamma-irradiated A549 cells at 24 h after irradiation.

| PRJNA445849 | ENA

The HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR mutated and wildtype NSCLC cells

Project description:The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs), such as erlotinib. Chromatin-modifying agents offer a novel therapy approach by sensitizing tumor cells to TKIs. The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) and NCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation were quantified by WST-1 assay, apoptosis by Annexin V/7-AAD flow cytometry and histone marks (acH3, H3K4me1,-2,-3) by immunoblotting. Expectedly, the EGFR wt cell lines A549 and NCI-H460 were insensitive to the growth-inhibiting effect of single-agent erlotinib (IC50 70-100µM), compared to HCC827 (IC50 <0.02μM). Treatment with panobinostat diminished growth to <50% in both EGFR wt and <30% in HCC827 cells. The combination of both drugs significantly reduced proliferation by ≥70% in A549, >95% in HCC827, but not further in NCI-H460. Panobinostat alone induced differentiation and expression of p21WAF1/CIP1 and p53 in all three cell lines, with almost no further increase when combined with erlotinib. In contrast, combination treatment additively decreased pERK, pAKT and pEGFR in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we also saw an induction of H3K4 methylation marks in all three cell lines. In conclusion, panobinostat synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in adenocarcinoma EGFR wt patients, combination therapy with an HDACi might offer a promising therapy approach to extend this activity. Copy-number analysis of three NSCLC cell lines HCC827, A549 and NCI-H460 (in unicates) was performed according to protocol by Affymetrix Genome-Wide Human SNP-Array 6.0.

2014-12-03 | E-GEOD-63784 | biostudies-arrayexpress

ChIP-seq from A549 (ENCSR871XML)

Project description:rabbit-IgG-control ChIP-seq on human A549 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2017-01-04 | GSE92122 | GEO

Homo sapiens

Project description:Expression data from mRNA in complex with EGFR from irradiated human A549 (ATCC CCL185) cells

| PRJNA357552 | ENA

H3K27ac, H3K4me3 ChIPseq of A549 (T/T) and A549 (C/C) cells

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications, H3K27ac, H3K4me3 in A549 (T/T) and A549 (C/C) cells;

2023-05-10 | GSE225332 | 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