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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

Project description:Effect of testosterone treatment on gene expression of lung adenocarcinoma derived cell line A549

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

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

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

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Transcription profiling of human GRE specific DNA-binding polyamide effect on dexamethasone-stimulated lung adenocarcinoma cell line

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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.

Project description:Purpose:This study aims to investigate the potential role of DUS4L (dihydrouridine synthase 4 like) in lung adenocarcinoma (LUAD) and explore its associated pathways in human LUAD. Methods:Firstly, we evaluated the relationships between clinicopathological characteristics and DUS4L expression via analysis of TCGA RNA sequencing data and other publicly available databases. Then, DUS4L was effectively silenced in LUAD cell line A549 using the lentiviral shRNA (short-hairpin RNA) transfection to assess its effects on cell proliferation, cycle and apoptosis in LUAD cells. RNA-seq technology was applied to shDUS4L and shCtrl-transfected cells to generate the corresponding gene expression profiles. Differentially expressed genes (DEGs) were identified using the DESeq2 program package. Also, DEGs were subjected to Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis to explore the associated molecular signaling pathways and relevant biological functions. Results:Analysis of TCGA data revealed that DUS4L was highly upregulated in LUAD tissues which was related to clinical T and TNM stages of LUAD. The knockdown of DUS4L effectively inhibited cell proliferation and promoted apoptosis in A549 cells. Furthermore, the DEGs between the shDUS4L and shCtrl A549 cells were mainly enriched in biological processes associated with spliceosome, ribosome, RNA catabolic process, ncRNA (non-coding RNA) processing, and p53 signaling pathway. Conclusion:Altogether, our results suggest that DUS4L is significantly associated with tumorigenesis and could be utilized as a novel biomarker and therapeutic target for LUAD.

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