Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene expression profiling in A549 cells exposed to TCDD and BaP for 2 weeks

ABSTRACT: Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, and BaP for 2w Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, and compare them with changes in transcriptome of A549 cells exposed to BaP for 2w.

ORGANISM(S): Homo sapiens

PROVIDER: GSE122733 | GEO | 2019/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Global gene expression profiling in A549 cells exposed to TCDD, CH223191 or TCDD+CH223191 for 6 h

Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, CH223191 or their combination Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, both sensitive and non-sensitive to co-treatment with AhR inhibitor CH223191. Comparison of our data with results from previously reported microarray and ChIP-seq experiments enabled us i) to identify candidate genes, which expression status acutely (e.g. Aldh1a3, Grem1, Hipk2, Tiparp), or with a delay (Cdh1, Dkk1, Bmp6), reflects exposure of lung cancer cells to TCDD, ii) to predict processes/pathways (e.g. ER stress, Wnt/β-cat, IFNɣ, EGFR/Erbb1), as well as iii) putative TFs (e.g. Stat, AP1, E2F1, TCF4), which may be implicated in adaptive response of lung cells to TCDD-induced AhR activation.

2018-01-25 | GSE109576 | GEO

Global gene expression profiling in A549 cells exposed to TCDD and BaP for 2 weeks

Project description:Global gene expression profiling in A549 cells exposed to TCDD and BaP for 2 weeks

| PRJNA506203 | ENA

Transcription profiling of human wild type and mutant hepatoma cells botg ligand-activated and -unactivated AHR

Project description:Starting with our early global expression analyses of TCDD-treated human hepatoma cells {Puga, 2000 4679 /id}, the AHR transcriptional induction profile has been extensively studied, whether activated by TCDD, B[a]P or in the absence of exogenous ligands (reviewed in {Frericks, 2007 5618 /id}). In addition to using prior knowledge to integrate expression profiles into the AHR gene target network, we performed a new set of expression profile analyses of wild type Hepa-1c1c7 and c35 cell lines and compared the responses in naÃ¯ve cells with responses in TCDD or B[a]P exposed cells for 8 hours. Results of our expression array studies are in close agreement with current knowledge. Experiment Overall Design: Three biological replicates were each performed for wildype naÃ¯ve cells (DMSO), TCDD activated cells, and B[a]P activated cells, and for c35 (AHR mutant) naÃ¯ve cells (DMSO), TCDD activated cells, and B[a]P activated cells.

2009-04-25 | E-GEOD-11796 | biostudies-arrayexpress

Microarray analysis of gene expression in human bronchial epithelial cells exposed to arsenic, BaP alone or arsenic plus BaP

Project description:Human bronchial epithelial cell BEAS-2B cells were continuously exposed to a vehicel control (DMSO), arsenic (NaAsO2, 1 uM), BaP (2.5 um) alone or arsenic plus BaP for 30 weeks. At the end of exposure, cells were collected and total RNA was extracted for microarray analysis.

2022-05-18 | GSE149605 | GEO

ligand-activated and -unactivated AHR in wiltype and mutant hepatoma cells

Project description:Starting with our early global expression analyses of TCDD-treated human hepatoma cells {Puga, 2000 4679 /id}, the AHR transcriptional induction profile has been extensively studied, whether activated by TCDD, B[a]P or in the absence of exogenous ligands (reviewed in {Frericks, 2007 5618 /id}). In addition to using prior knowledge to integrate expression profiles into the AHR gene target network, we performed a new set of expression profile analyses of wild type Hepa-1c1c7 and c35 cell lines and compared the responses in naïve cells with responses in TCDD or B[a]P exposed cells for 8 hours. Results of our expression array studies are in close agreement with current knowledge.

2009-04-17 | GSE11796 | GEO

TCDD exposure in control and slincR zebrafish morphants at 48 hpf

Project description:Background: A structurally diverse group of chemicals, including polycyclic aromatic hydrocarbons (PAHs), can inappropriately activate the aryl hydrocarbon receptor (AHR) and lead to adverse health effects. In the zebrafish model, repression of sox9b has a causal role in several AHR-mediated toxic responses, including craniofacial cartilage malformations; however, the mechanism of sox9b repression remains unknown. We previously identified a long non-coding RNA, slincR, which is increased (in an AHR-dependent manner) by multiple AHR ligands and is required for the AHR-activated repression of sox9b. Objective: Enhance our understanding of the signaling events downstream of AHR activation that contribute to toxic responses. To understand slincR’s role in the TCDD-induced toxicity pathway, we performed RNA-sequencing and gene ontology enrichment analysis on 48 hpf control and slincR morphants exposed to 0.1% DMSO or 1 ng/mL TCDD.

2018-10-25 | GSE106131 | GEO

Thalassiosira pseudonana exposure to benzopyrene BaP

Project description:Comparison of transcriptional profile of Thalassiosira pseudonana exposed for 24h to 36.45 ug/L BaP and methanol-treated controls. Four biological replicates (BaP treatment) and six biological replicates (controls).

2012-02-15 | E-MEXP-3558 | biostudies-arrayexpress

Expression profiling of four replicates of MCF-7 cells treated with 100nM TCDD

Project description:The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that binds pollutants, therapeutic drugs and endogenous ligands. The AHR is expressed in all breast cancer subtypes and it can switch the aggressiveness of breast cancer cells from low to high depending on the ligand that it binds. Jagged 1 (JAG1) is a NOTCH receptor ligand that is overexpressed in basal-like breast cancer. JAG1 promotes breast cancer progression in part by increasing the migratory and invasive activity of breast cancer cells (BCCs). The regulation of JAG1 by AHR in MCF-7 and MDA-MB-231 BCCs by two AHR ligands (TCDD and ITE) was investigated in this report. TCDD is the prototype AHR ligand, and ITE is a non-toxic endogenous AHR ligand with anti-cancer activity. Ingenuity pathway analysis (IPA) revealed a significant association between TCDD-regulated genes (TRGs) and cell movement. Short interfering RNA (siRNA)-directed knockdown of AHR confirmed TCDD-stimulated decreases in JAG1 required AHR expression. TCDD-induced reductions in JAG1 were inhibited by the AHR antagonist CH-223191. The endogenous non-toxic AHR ligand ITE also reduced JAG1 by activating AHR in BCCs. MDA-MB-231 are basal-like BCCs that are highly migratory and invasive, and these cancer cell attributes were significantly inhibited by ITE. We reduced JAG1 with targeting siRNA, and the outcome mirrored ITE, it suppressed TNBC cell migration and invasive activity. Collectively, these findings are the first showing that ITE is a tumor-suppressing AHR ligand in TNBC cells in part because it reduces JAG1 expression

2018-08-15 | GSE98514 | GEO

p53 status and BaP or BPDE gene expression response

Project description:Human colon carcinoma cells (HCT116) differing in p53 status were exposed to benzo(a)pyrene (BaP) (2.5 and 5 uM for up to 48 h) or anti-benzo(a)pyrene-trans-7,8-dihydrodiol-9,10-epoxide (BPDE)(0.5 and 1 uM for up to 24 h), and their gene expression responses compared by cDNA microarray technology. Keywords: BaP or BPDE exposure

2007-11-13 | GSE9547 | GEO

Effect of 13 weeks of subchronic exposure to TCDD, PeCDF, PCB126, PCB153 and PCB126/PCB153 on hepatic gene expression

Project description:This study investigates the effects of the aryl hydrocarbon receptor (AhR) ligands TCDD, PCB126 and PeCDF; the non-AhR ligand PCB153 and the binary mixture PCB126/PCB153 on hepatic gene expression in female sprague dawley rats. Rats were treated with toxicological equivalent doses of TCDD (100ng/kg), PeCDF (200ng/kg), PCB126 (1000ng/kg) and PCB153 (1000ug/kg) 5 days a week for 13 weeks. Keywords: Environmental pollutant toxicity comparison

2006-09-08 | GSE5789 | 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