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Tobacco smoke exposure-related pathway gene expression signature in the bronchial airway epithelium

ABSTRACT: Using primary human bronchial epithelial cells collected at bronchoscopy, we have perturbed signaling pathways important in regulation of response to tobacco smoke exposure and cancer development: ATM, BCL2, GPX1, NOS2, IKBKB, and SIRT1 Using gene expression profiles generated for each pathway and four independent gene expression datasets, we show that SIRT1 activity is significantly up-regulated in cytologically normal airway epithelial cells from active smokers compared to non-smokers; and in contrast, this activity is strikingly down-regulated in non-small cell lung cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37058 | GEO | 2012/09/27

SECONDARY ACCESSION(S): PRJNA158397

REPOSITORIES: GEO

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Tobacco smoke exposure-related pathway gene expression signature in the bronchial airway epithelium

Project description:Using primary human bronchial epithelial cells collected at bronchoscopy, we have perturbed signaling pathways important in regulation of response to tobacco smoke exposure and cancer development: ATM, BCL2, GPX1, NOS2, IKBKB, and SIRT1 Using gene expression profiles generated for each pathway and four independent gene expression datasets, we show that SIRT1 activity is significantly up-regulated in cytologically normal airway epithelial cells from active smokers compared to non-smokers; and in contrast, this activity is strikingly down-regulated in non-small cell lung cancer. 52 samples were run on Affymetrix Human Exon 1.0 ST microarrays (n=7 for ATM, n=8 for GPX1, n=7 for SIRT1, n=7 for NOS2, n=7 for IKBKB, n=8 for BCL2, and n=8 for GFP). The CEL files were processed using RMA and the ENTREZ Gene CDF file. 13 samples were removed either because of a low Pearson correlation between samples (n=1 SIRT1 sample) or a strong batch effect (n=2 ATM, n=2 BCL2, n=2 GFP, n=2 GPX1, n=1 IKBKB, n=2 NOS2, n=1 SIRT1 samples) as determined by PCA.

2012-09-27 | E-GEOD-37058 | biostudies-arrayexpress

Reversible and Permanent effects of Tobacco Smoke Exposure on Airway Epithelial Gene Expression

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

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PI3K pathway activity in the normal airway of smokers with lung cancer, and in smokers with airway dysplasia

2010-04-12 | GSE12815 | GEO

Transcription profiling of human airway epithelial cells to investigate the reversible and permanent effects of tobacco smoke exposure

2008-06-16 | E-GEOD-7895 | biostudies-arrayexpress

Threshold of Biologic Response of the Small Airway Epithelium to Low Levels of Tobacco Smoke

Project description:Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke. Affymetrix arrays were used to assess the gene expression data of smoking-responsive genes in the in small airway epithelium obtained by fiberoptic bronchoscopy of 48 healthy non-smokers (non-smoker or Nsaets), 65 healthy smokers (smoker), 7 symptomatic smokers (SYMs) and a healthy occasional smoker (OcSs). YSB and LO contributed equally to the study.

2011-02-02 | E-GEOD-19667 | biostudies-arrayexpress

Temporal RNA-sequencing of cytologically-normal mouse airway epithelia during tobacco carcinogen-associated lung tumorigenesis

Project description:Smoking perpetuates in cytologically-normal airways a molecular “field of injury” that is pertinent to lung cancer and early detection. The evolution of airway field changes prior to lung cancer onset is poorly understood largely due to the long latency of lung malignancy in smokers. Here we studied airway expression changes prior to lung cancer onset in mice with knockout of the Gprc5a gene and tobacco carcinogen (nicotine-specific nitrosamine ketone; NNK) exposure and that develop the most common type of lung cancer, lung adenocarcinoma (LUAD). Cytologically-normal airway epithelial brushings were collected before exposure and at multiple times following NNK exposure until time of LUAD development and then analyzed by RNA-sequencing (RNA-Seq).

2020-02-28 | GSE102707 | GEO

Airway epithelial cells from smokers treated with myo-inositol or placebo

Project description:Samples were obtained as part of a randomized, double blind, placebo-controlled, phase IIb study to determine the effects of myo-inositol in smokers with bronchial dysplasia. Smokers with greater than 1 site of dysplasia identified by autofluorescence bronchoscopy-directed biopsy were randomly assigned to receive oral placebo or myo-inositol, 9 g once/day for two weeks and then twice/day for 6 months. Cytologically normal airway epithelial cells were obtained via bronchoscopy from the right or left mainstem bronchus at baseline and 6 months post-treatment with myo-inositol or placebo from 69 study participants (n=138 samples). The RNA from these samples was isolated and used to prepare libraries for mRNA sequencing. Subjects were classified by response according to their change in dysplasia rate after 6-months. Among subjects with a complete response in the myo-inositol arm, there was a significant decrease in a gene expression signature reflective of PI3K activation.

2016-09-26 | GSE86422 | GEO

PI3K pathway activity in the normal airway of smokers with lung cancer, and in smokers with airway dysplasia

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. This study contains: 2 arrays from smokers with COPD (no lung cancer), 1 array from smoker without COPD (no lung cancer); 2 samples from patients with lung cancer, 2 samples from patients without lung cancer; 20 samples from 10 matched individuals with airway dysplasia before and after treatment with myo-inositol, 6 additional samples from individuals with airway dysplasia; 27 samples from mammary epithelial cells used in oncogenic pathway analysis that have either the PI3K pathway activated, the Np63 pathway activated, or are a GFP control.

2010-04-11 | E-GEOD-12815 | biostudies-arrayexpress

Threshold of Biologic Response of the Small Airway Epithelium to Low Levels of Tobacco Smoke

2011-02-02 | GSE19667 | GEO

mRNA-seq of Human Airway Epithelial Cells

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

2011-06-01 | GSE29006 | GEO

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