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Transcriptome of non-involved lung parenchyma from ever and never smoker lung adenocarcinoma patients from Milan, Italy.

ABSTRACT: Alteration of gene expression profile of target organs may signal exposure of that organ to toxic chemicals. We analyzed the transcriptome of the non-involved lung tissue, excised from 176 surgically treated lung adenocarcinoma patients, to identify genes whose expression levels were altered by individual habit to cigarette smoking. Of 17.097 genes analyzed, 357 resulted to be differentially expressed between never smokers and ever smokers (FDR <0.05). The gene that resulted to be the most significantly differentially expressed was MYO1A (FDR = 6.9 x 10-4 and ever versus never smokers fold change of 1.42). We compared our results with those of five independent datasets and found that more than one third (38.6%) of the transcripts associated with smoking habit in our dataset overlapped with at least one of the other datasets, with 7 genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) resulting significantly differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers than in never smokers. Most of the genes that we found significantly differentially expressed between ever and never smokers participate in pathways/networks that are directly or indirectly associated with immunity and inflammation, in particular, the most significantly enriched pathway was that of eicosanoid signaling. Overall, present results further points to the inflammatory condition that characterize the lung tissue of smokers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123352 | GEO | 2019/10/01

REPOSITORIES: GEO

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A Pilot Study Of Immunological and Microbiome Profiling Reveals Distinct Inflammatory Profiles For Smokers and Electronic Cigarette Users [re-analysis]

Project description:Background: Smoking increases pulmonary inflammation, but an effect by electronic cigarette (EC) vaping is less understood. We previously reported smokers (SM) had increased lung immune cell counts and inflammatory gene expression in bronchial epithelial cells compared to EC users and never-smokers (NS). Here we report association of smoking and vaping with immune cell subtypes and gene expression in bronchoalveolar lavage. Methods: SM, EC users, and NS underwent bronchoscopy (n=28). RNASeq and the CIBERSORT computational algorithm were used to determine immune cell subtypes, along with inflammatory gene expression and microbiome metatranscriptomics. Correlations and associations were assessed across and within the tobacco-use groups, corrected for false discovery rates. Results: Classification of macrophage subtypes revealed a 2-fold increase in M0 macrophages for smokers and EC users relative to never-smokers, with a concordant decrease in M2 macrophages. There were 68, 19, and 1 significantly differentially expressed inflammatory genes (DEG) (FDR<0.05; log2-fold change>1) between SM/NS, SM/EC users, and EC users/NS respectively. CSF-1 and GATA3 expression correlated positively and inversely with M0 and M2 macrophages respectively. Correlation profiling for DEG showed distinct lung profiles for each participant group. There were 3 bacteria genera-DEG correlations and 3 bacteria genera-macrophage subtype correlations (Diffcorr>0.5 and FDR<0.1). Conclusions: In this pilot study, smoking and EC use were associated with an increase in undifferentiated M0 macrophages, but smokers differed from EC users and NS for inflammatory gene expression. The preliminary data support the hypothesis that smoking and EC use have toxic lung effects influencing inflammatory responses, but not via changes in the microbiome.

2023-07-05 | GSE227547 | GEO

Smoking induced expression of the GPR15 gene indicates its potential role in chronic inflammatory pathologies

Project description:The aim of present study was to study the changes in peripheral blood gene expression profile induced by smoking. RNA was extracted from the PBMCs of 48 persons with detailed smoking history (24 were non-smokers, 16 were current smokers and 8 were ex-smokers). Gene expression profile was evaluated with the RNA sequencing and results were analyzed separately in males (24) and females (24). In male smokers, 13 genes were statistically significantly (FDR < 0.1) differentially expressed. In female smoker, 5 genes were differentially expressed with the FDR<0.1. Most of the differentially expressed genes were different between male and female smokers. However, GPR15, expression was changed in male and female smokers compared to non-smokers. Further analysis on the methylation of the genes GPR15 identified significant hypomethylation in smokers compared to non-smokers. GPR15 is the chemo-attractant receptor that regulates T-cell migration and immunity. Up-regulation of GPR15 could explain to some extend the health hazards of smoking for chronic inflammatory diseases

2018-04-30 | GSE68549 | GEO

Smoking Status Impacts microRNA Mediated Prognosis and Lung Adenocarcinoma Biology

Project description:Cigarette smoke is associated with the majority of lung cancers: however, 25% of lung cancer patients are non-smokers, and half of all newly diagnosed lung cancer patients are former smokers. Lung tumors exhibit distinct epidemiological, clinical, pathological, and molecular features depending on smoking status, suggesting divergent mechanisms underlie tumorigenesis in smokers and non-smokers. MicroRNAs (miRNAs) are integral contributors to tumorigenesis and mediate biological responses to smoking. Based on the hypothesis that smoking-specific miRNA differences in lung adenocarcinomas reflect distinct tumorigenic processes selected by different smoking and non-smoking environments, we investigated the contribution of miRNA disruption to lung tumor biology and patient outcome in the context of smoking status. Results: We discovered novel and distinct smoking-status-specific patterns of miRNA and miRNA-mediated gene networks, and identified miRNAs that were prognostically significant in a smoking-dependent manner. Conclusions: We conclude that miRNAs disrupted in a smoking-status-dependent manner affect distinct cellular pathways and differentially influence lung cancer patient prognosis in current, former and never smokers. Our findings may represent promising biologically relevant markers for lung cancer prognosis or therapeutic intervention. We applied a whole transcriptome sequencing based approach to interrogate miRNA levels in 94 patient-matched lung adenocarcinoma and non-malignant lung parenchymal tissue pairs from current [CS], former [FS] and never smokers [NS].

2014-10-30 | E-GEOD-62182 | biostudies-arrayexpress

Persistence of Smoking-induced Dysregulation of Small Airway Epithelium miRNA Expression Despite Smoking Cessation

Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders.

2015-11-23 | GSE53519 | GEO

Antioxidant response gene expression in the bronchial airway epithelial cells of smokers at risk for lung cancer

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

Smoking Status Impacts microRNA Mediated Prognosis and Lung Adenocarcinoma Biology

2014-10-30 | GSE62182 | GEO

Persistence of Smoking-induced Dysregulation of Small Airway Epithelium miRNA Expression Despite Smoking Cessation

Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/Î²-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders. MicroRNA profiling identified 34 miRNAs up-regulated by cigarette smoking in human small airway epithelium. Even after quitting smoking for 3 months, 12 miRNAs didnât return to normal level.

2015-11-23 | E-GEOD-53519 | biostudies-arrayexpress

Antioxidant response gene expression in the bronchial airway epithelial cells of smokers at risk for lung cancer

2010-10-01 | GSE19027 | GEO

Analysis of miRNA expression profiling in 3 samples(normal, cigarette smoking and lung cancer population's serum)

Project description:Using the highly sensitive miRNA array, we determined the serum miRNAs profiles of 10 non-smokers, 10 smokers and 10 lung cancer patients by miRCURY LNA™ microRNA Arrays. Differential expressed miRNAs were further validated in a larger scale samples. We found that let-7i-3p and miR-154-5p were significantly downregulation in serum of smokers and lung cancer patients. The serum level of let-7i-3p and miR-154-5p is associated with smoking and smoking-related lung cancer.

2014-06-17 | GSE58540 | GEO

DNA Methylation and RNA Expression Profiles in Lung Adenocarcinomas [DNA methylation]

Project description:Lung cancer occurs in never-smokers. Epigenetic changes in lung cancer potentially represent important diagnostic, prognostic, and therapeutic targets. We compared DNA methylation profiles of 28 adenocarcinomas of the lungs of never-smokers with paired adjacent nonmalignant lung tissue. We correlated differential methylation changes with gene expression changes from the same 28 samples. We observed a distinct separation in methylation profiles between tumor and adjacent nonmalignant lung tissue using principal component analysis. Tumors were generally hypomethylated compared with adjacent nonmalignant tissue. Of 1,906 differentially methylated CpG sites between tumor and nonmalignant tissue, 1,198 were within classically defined CpG islands where tumors were hypermethylated compared with nonmalignant tissue. A total of 708 sites were outside CpG islands where tumors were hypomethylated compared with nonmalignant tissue. There were significant differences in expression of 351 genes (23%) of the 1,522 genes matched to the differentially methylated CpG sites. Genes that were not significantly differentially expressed and were hypermethylated within CpG sites were enriched for homeobox genes. These results suggest that the methylation profiles of lung adenocarcinomas of never-smokers and adjacent nonmalignant lung tissue are significantly different. Despite the differential methylation of homeobox genes, no significant changes in expression of these genes were detected. Twenty eight pairs of tumor and adjacent normal lungs were profiled for lung adenocarcinoma patients by gene expression and DNA methylation microarray

2015-02-03 | E-GEOD-62948 | biostudies-arrayexpress

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