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Transcription profiling of human lung adenocarcinoma derived cell line A549 treated with dexamethasone

ABSTRACT: Effect of dexamethasone on gene expression in lung adenocarcinoma derived cell line A549

ORGANISM(S): Homo sapiens

SUBMITTER: Mikkonen Laura

PROVIDER: S-ECPF-MEXP-2004 | biostudies-other |

REPOSITORIES: biostudies-other

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Transcription profiling of human lung adenocarcinoma derived cell line A549 treated with testosterone

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Transcription profiling of human lung adenocarcinoma derived cell line A549 treated with dexamethasone

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Transcription profiling of human A549 lung adenocarcinoma cell line time Course of TGF-beta treatment

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Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Transforming growth factor-? impairs glucocorticoid activity in the A549 lung adenocarcinoma cell line.

Project description:Background and purposeThe lung adenocarcinoma cell line, A549, undergoes epithelial-mesenchymal cell transition (EMT) in response to TGF-?. Glucocorticoids do not prevent the EMT response, but TGF-? induced resistance to the cytokine-regulatory action of glucocorticoids. We sought to characterize the impairment of glucocorticoid response in A549 cells.Experimental approachA549 cells were exposed to TGF-? for up to 96?h before glucocorticoid treatment and challenge with IL-1? to assess glucocorticoid regulation of IL-6 and CXCL8 production. Nuclear localization of the glucocorticoid receptor ? (GR?) was ascertained by immunofluorescence and Western blotting. Transactivation of the glucocorticoid response element (GRE) was measured with a transfected GRE-secreted human placental alkaline phosphatase reporter.Key resultsTGF-? (40-400?pM) reduced the maximum inhibitory effect of dexamethasone on IL-1?-induced IL-6 and CXCL8 production. The impaired glucocorticoid response was detected with 4?h of TGF-? (40?pM) exposure (and 4?h IL-1? to induce CXCL8 expression) and therefore was not secondary to EMT, a process that requires longer incubation periods and higher concentrations of TGF-?. TGF-? also impaired dexamethasone regulation of granulocyte-macrophage colony-stimulating factor in thrombin-stimulated BEAS-2B epithelial cells. Impaired regulation of CXCL8 was associated with markedly reduced GRE transactivation and reduced induction of mRNA for I?B?, the glucocorticoid-inducible leucine zipper and the epithelial sodium channel (SCNN1A). The expression, cellular levels and nuclear localization of GR? were reduced by TGF-?.Conclusions and implicationsWe have identified mechanisms underlying the impairment of responses to glucocorticoids by TGF-? in the A549 and BEAS-2B cell lines.

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DUS4L Silencing Suppresses Cell Proliferation and Promotes Apoptosis in Human Lung Adenocarcinoma Cell Line A549.

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