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Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1

ABSTRACT: We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1. In this dataset, we include the expression data obtained from A549 cells after treatment with purified flagellin or transforming growth factor beta 1 receptor. The analysis indicated that flagellin induced a change in gene expression that was similar to the changes induced by transforming growth factor 1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38309 | GEO | 2012/10/31

SECONDARY ACCESSION(S): PRJNA167617

REPOSITORIES: GEO

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Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1

Project description:We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1. In this dataset, we include the expression data obtained from A549 cells after treatment with purified flagellin or transforming growth factor beta 1 receptor. The analysis indicated that flagellin induced a change in gene expression that was similar to the changes induced by transforming growth factor 1. A549 cells were treated with flagellin or transforming growth factor 1 for 24 h. Total RNA was extracted and reverse transcribed to cDNA. Synthesized cDNA was fragmented and labeled with biotin. The biotinylated cDNA was hybridized to to an Affymetrix GeneChip Array, and probe signal intensities were captured.

2012-10-31 | E-GEOD-38309 | biostudies-arrayexpress

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Project description:Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1

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RNA-seq analysis of A549 cells harboring Smad3 R104K A105P mutation.

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Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.

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Project description:Epithelial–mesenchymal transition (EMT) is a plastic process that converts epithelial cells into migratory and invasive cells. Accumulating evidence indicates that EMT is a key event for metastasis in several types of cancer, including non-small cell lung cancer (NSCLC). Especially, transforming growth factor-beta (TGF-beta) acts as a potent inducer of EMT and contributes to cancer progression. Emerging studies suggest that a metabolic reprograming is essential to acquire the EMT phenotype in cancer cells. However, a comprehensive understanding of metabolism in cancer EMT remains largely unexplored. Here, we analyzed metabolic changes during TGF-beta-induced EMT in NSCLC A549 cells using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS). At the same time, we examined the expression of metabolic-related genes using microarray analysis.

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