MRNA-seq of Human Airway Epithelial Cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE29006 | GEO | 2011/06/01
SECONDARY ACCESSION(S): PRJNA153969
REPOSITORIES: GEO
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Project description:mRNA expression was profiled from pooled bronchial airway epithelial cell brushings (n=3 patients/pool) obtained during bronchoscopy from healthy never (NS) and current smokers (S) and smokers with (C) and without (NC) lung cancer 4 samples were sequened, each representing a pool of 3 patients. The phenotypes of the 4 samples were as follows: healthy non-smoker, healthy smoker, smoker without lung cancer and smoker with lung cancer.
2011-06-01 | E-GEOD-29006 | biostudies-arrayexpress
Project description:Smoking is a significant risk factor for lung cancer, the leading cause of cancer-related deaths worldwide. While microRNAs are regulators of many airway gene-expression changes induced by smoking, their role in modulating changes associated with lung cancer in these cells remains unknown. Here, we use next-generation sequencing of small RNAs in the airway to identify miR-4423 as a novel primate-specific microRNA associated with lung cancer and expressed primarily in mucociliary epithelium. The endogenous expression of miR-4423 increases as bronchial epithelial cells undergo differentiation into mucociliary epithelium in vitro and its overexpression during this process causes an increase in the number of ciliated cells. Furthermore, expression of miR-4423 is reduced in most lung tumors and in cytologically normal epithelium of the mainstem bronchus of smokers with lung cancer. In addition, ectopic expression of miR-4423 in a subset of lung cancer cell lines reduces their anchorage-independent growth and significantly decreases the size of the tumors formed in a mouse xenograft model. Consistent with these phenotypes, overexpression of miR-4423 induces a differentiated-like pattern of airway epithelium gene expression and reverses the expression of many genes that are altered in lung cancer. Together, our results indicate that miR-4423 is a novel regulator of airway epithelium differentiation and that the abrogation of its function contributes to lung carcinogenesis. Small RNA expression was profiled from pooled bronchial airway epithelial cell brushings (n=3 patients/pool) obtained during bronchoscopy from healthy never (NS) and current smokers (S) and smokers with (C) and without (NC) lung cancer. MicroRNA hsa-miR-4423 was over expressed in H1299, Calu6, SW900 and H2170 lung cancer cell lines.
2013-10-08 | E-GEOD-48796 | biostudies-arrayexpress
Project description:Smoking is a significant risk factor for lung cancer, the leading cause of cancer-related deaths worldwide. While microRNAs are regulators of many airway gene-expression changes induced by smoking, their role in modulating changes associated with lung cancer in these cells remains unknown. Here, we use next-generation sequencing of small RNAs in the airway to identify miR-4423 as a novel primate-specific microRNA associated with lung cancer and expressed primarily in mucociliary epithelium. The endogenous expression of miR-4423 increases as bronchial epithelial cells undergo differentiation into mucociliary epithelium in vitro and its overexpression during this process causes an increase in the number of ciliated cells. Furthermore, expression of miR-4423 is reduced in most lung tumors and in cytologically normal epithelium of the mainstem bronchus of smokers with lung cancer. In addition, ectopic expression of miR-4423 in a subset of lung cancer cell lines reduces their anchorage-independent growth and significantly decreases the size of the tumors formed in a mouse xenograft model. Consistent with these phenotypes, overexpression of miR-4423 induces a differentiated-like pattern of airway epithelium gene expression and reverses the expression of many genes that are altered in lung cancer. Together, our results indicate that miR-4423 is a novel regulator of airway epithelium differentiation and that the abrogation of its function contributes to lung carcinogenesis. Small RNA expression was profiled from pooled bronchial airway epithelial cell brushings (n=3 patients/pool) obtained during bronchoscopy from healthy never (NS) and current smokers (S) and smokers with (C) and without (NC) lung cancer. MicroRNA hsa-miR-4423 was over expressed in H1299, Calu6, SW900 and H2170 lung cancer cell lines.
2013-10-08 | E-GEOD-32726 | biostudies-arrayexpress
Project description:Prior microarray studies of smokers at high risk for lung cancer have demonstrated that heterogeneity in bronchial airway epithelial cell gene expression response to smoking can serve as an early diagnostic biomarker for lung cancer. This study examines the relationship between gene expression variation and genetic variation in a central molecular pathway (NRF2-mediated antioxidant response) associated with smoking exposure and lung cancer. We assessed global gene expression in histologically normal airway epithelial cells obtained at bronchoscopy from smokers who developed lung cancer (SC, n=20), smokers without lung cancer (SNC, n=24), and never smokers (NS, n=8). Functional enrichment showed that the NRF2-mediated antioxidant response pathway differed significantly among these groups. Keywords: Global mRNA expression profiling 21 total arrays (20 unique patients) run on total RNA obtained from Bronchial Epithelium of Smokers with Lung Cancer 30 total arrays (24 unique patients) run on total RNA obtained from Bronchial Epithelium of Smokers without Lung Cancer 9 total arrays (8 unique patients) run on total RNA obtained from Bronchial Epithelium of Never Smokers
2010-09-30 | E-GEOD-19027 | biostudies-arrayexpress
Project description:Prior microarray studies of smokers at high risk for lung cancer have demonstrated that heterogeneity in bronchial airway epithelial cell gene expression response to smoking can serve as an early diagnostic biomarker for lung cancer. This study examines the relationship between gene expression variation and genetic variation in a central molecular pathway (NRF2-mediated antioxidant response) associated with smoking exposure and lung cancer. We assessed global gene expression in histologically normal airway epithelial cells obtained at bronchoscopy from smokers who developed lung cancer (SC, n=20), smokers without lung cancer (SNC, n=24), and never smokers (NS, n=8). Functional enrichment showed that the NRF2-mediated antioxidant response pathway differed significantly among these groups. Keywords: Global mRNA expression profiling
2010-10-01 | GSE19027 | GEO
Project description:MicroRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine the effect of cigarette smoke exposure on airway epithelial microRNA expression Keywords: Global microRNA expression profiling Bronchial epithelial cells were collected from current and never smokers via bronchoscopy. Low molecular weight RNA ( < 200 nucleotides) was isolated and hybridized to Invitrogen NCode microRNA microarrays to determine which microRNAs detected in bronchial epithelial cells were differentially expressed in the airways of smokers.
2009-01-28 | E-GEOD-14634 | biostudies-arrayexpress
Project description:RNA was obtained from histologically normal bronchial epithelium of never, former, and current smokers undergoing fiberoptic bronchoscopy. Statistical analysis of the gene expression data identified gene differentially expressed between current and never smokers and classified these genes as irreversible, slowly reversible, or rapidly reversible based on their behavior in former smokers Experiment Overall Design: Microarrays run on total RNA obtained from Bronchial Epithelium of Never Smokers (n=21), Former Smokers (n=31), and Current Smokers (n=52)
2008-06-16 | E-GEOD-7895 | biostudies-arrayexpress
Project description:RNA was obtained from histologically normal bronchial epithelium of never, former, and current smokers undergoing fiberoptic bronchoscopy. Statistical analysis of the gene expression data identified gene differentially expressed between current and never smokers and classified these genes as irreversible, slowly reversible, or rapidly reversible based on their behavior in former smokers Keywords: Disease state analysis
2007-10-02 | GSE7895 | GEO
Project description:BACKGROUND: We have previously reported gene expression changes in the bronchial airway epithelium of active chronic smokers. In this study, we investigate the effects of Acute Smoke Exposure (ASE) from cigarettes on airway epithelial gene expression. METHODS: Bronchial airway epithelial cell brushings were collected via fiberoptic bronchoscopy from 63 individuals without recent exposure to cigarette smoke (> 2 days), at baseline and at 24 hours after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Differential gene expression was assessed using linear modeling and compared to previous smoking-related gene-expression signatures using Gene Set Enrichment Analysis (GSEA). RESULTS: We identified 91 genes differentially expressed 24-hours after exposure to three cigarettes (FDR < 0.25). ASE induces genes involved in xenobiotic metabolism, oxidative stress, and inflammation; and represses genes involved in cilium morphogenesis, and cell cycle. Genes induced by in vivo ASE are concordantly altered by ASE in vitro. While many genes altered by ASE are altered similarly in the airway of chronic smokers, metallothionein genes were induced by ASE and suppressed among chronic smokers. Metallothioneins were also suppressed in the bronchial airway of current and former chronic smokers with lung cancer relative to those with benign disease. CONCLUSIONS: Acute exposure to as little as three cigarettes alters gene-expression in bronchial airway epithelium in a manner that largely resembles the changes seen in chronic active smokers. The difference in the short-term and long-term effects of smoking on metallothionein expression and its relationship to lung cancer requires further study given these enzymes’ role in responding to oxidative stress.
2018-06-26 | GSE97010 | GEO
Project description:Cytologically normal airway epithelial samples were collected during bronchoscopy of current and former smokers. Subjects enrolled in this study were either under suspicion of having lung cancer, had dysplasia in their airway, or were a healthy current, former or never smoker. We supplemented existing GEO series (GSE4115 and GSE7895) with the samples in this study to explore PI3K pathway activity in the these cohorts.
2010-04-12 | GSE12815 | GEO