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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109576 | GEO | 2018/01/25

REPOSITORIES: GEO

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

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

| PRJNA431419 | ENA

Deletion of TIPARP increases sensitivity to dioxin-induced hepatosteatosis and lethality

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