Ontology highlight
ABSTRACT:
PROVIDER: PRJNA398169 | ENA |
REPOSITORIES: ENA
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Project description:Tobacco is mainly consumed in two different forms (smoking and chewing) that vary in their composition and methods of intake. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon tobacco exposure are yet to be fully elucidated. We therefore sought to compare the molecular alterations in oral keratinocytes exposed to smoke and chewing tobacco. OKF6/TERT1 cells were exposed to cigarette smoke condensate or chewing tobacco for progressively increasing durations (2, 4, 6 and 8 months). We employed a TMT-based quantitative proteomics approach to investigate the adverse effects of chronic cigarette smoke or chewing tobacco exposure in oral keratinocytes. LC/MS3 analysis resulted in the quantification of 5,342 proteins and 2,821 proteins in cigarette smoke and chewing tobacco exposed cells, respectively. Upstream regulator analysis indicates the involvement of distinct regulators in CSC exposed cells compared to STE exposed cells. In addition, exome sequencing revealed discrete genetic alterations in cells exposed to each insult. Current analysis defines a clear distinction in the molecular dysregulation in oral cells in response to different tobacco-based insults. Some of the proteins dysregulated in cigarette smoke or chewing tobacco exposed cells may serve as potential early detection biomarkers which could aid in stratification of patients based on tobacco usage history.
2019-11-08 | PXD007127 | Pride
Project description:Tobacco in its smoke and smokeless form are major risk factors for ESCC (esophageal squamous cell carcinoma). However, molecular alterations associated with smokeless tobacco exposure are poorly understood. In the Indian subcontinent, tobacco is predominantly consumed in chewing form. An understanding of molecular alterations associated with chewing tobacco exposure is vital for identifying molecular markers and potential targets. We developed an in-vitro cellular model by exposing non-transformed esophageal epithelial cells to chewing tobacco over eight month period. Chronic exposure to chewing tobacco led to increase in cell proliferation, invasive ability and anchorage independent growth indicating cell transformation. Molecular alterations associated with chewing tobacco exposure were characterized by carrying out exome sequencing and quantitative proteomic profiling of parental cells and chewing tobacco exposed cells. Quantitative proteomic analysis revealed that established cancer stem cell markers are elevated in tobacco treated cells. Decreased expression of enzymes associated with the glycolytic pathway and increased expression of a large number of mitochondrially localized proteins involved in the electron transport chain as well as enzymes of TCA cycle were also identified. Electron micrographs revealed increase in number and size of mitochondria. Based on these observations, we hypothesise that chronic treatment of esophageal epithelial cells with tobacco leads to a cancer stem cell-like phenotype. These cells also show characteristic OXPHOS phenotype which can be potentially targeted as a therapeutic strategy.
2019-11-11 | PXD013396 | Pride
Project description:Gene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays. Keywords: time course, cigarette smoke exposure
2008-03-04 | GSE10700 | GEO
Project description:Cigarette smoke (CS) causes adverse health effects and leads to the development of respiratory disease (chronic obstructive pulmonary disease), cardiovascular disease, and cancer. To reduce the risk of smokers developing smoking-related diseases, Philip Morris International is developing modified risk tobacco products (MRTP). Within a systems toxicology study, we conducted an integrative multi-omics analysis to assess the effects of aerosols from two potential MRTPs - the Carbon Heated Tobacco Product (CHTP) 1.2 and the Tobacco Heating System (THS) 1.2 -, compared with cigarette smoke (CS) at matched nicotine concentrations, on the lung of ApoE-/- mice. Mice were exposed for up to six months and molecular exposure effects were measured by mRNA/miRNA transcriptomics, proteomics, metabolomics, and lipidomics. In addition, the impact of cessation (CESS) or switching to CHTP 1.2 (SWITCH) after three months of CS exposure was evaluated. This data set represents the lung metabolomics data obtained after 3 and 6 months of exposure. The 'Animal ID' or 'CAN' represents the unique animal identifier and allows matching of samples across the different data modalities.
2020-04-25 | MTBLS158 | MetaboLights
Project description:Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.
2016-10-12 | GSE82137 | GEO
Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course
2005-02-23 | GSE2302 | GEO
Project description:Gene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays. Experiment Overall Design: 4 replicate Petri dishes of cells were exposed in a custom-built smoke exposure chamber. Cigarettes were smoked as per FTC protocols, and the smoke diluted such that the cells were at least 50% viable as compared to mock (air)-exposed controls after 24h. RNA from each replicate dish was analyzed using a separate array. Four replicates of an incubator (untreated with either smoke or air) are included also.
2008-04-06 | E-GEOD-10700 | biostudies-arrayexpress
Project description:This study reports a comparative assessment of the biological impact of a heated tobacco aerosol from the tobacco heating system (THS) 2.2 and smoke from a combustible 3R4F cigarette. Human organotypic bronchial epithelial cultures were exposed to an aerosol from THS2.2 (a candidate modified-risk tobacco product) or 3R4F smoke at similar nicotine concentrations. A systems toxicology approach was applied to enable a comprehensive exposure impact assessment. Culture histology, cytotoxicity, secreted pro-inflammatory mediators, ciliary beating, and genome-wide mRNA/miRNA profiles were assessed at various time points post-exposure. Series of experimental repetitions were conducted to increase the robustness of the assessment. At similar nicotine concentrations, THS2.2 aerosol elicited lower cytotoxicity compared with 3R4F smoke. No morphological change was observed following exposure to THS2.2 aerosol, even at nicotine concentration three times that of 3R4F smoke. Lower levels of secreted mediators and fewer miRNA alterations were observed following exposure to THS2.2 aerosol than following 3R4F smoke. Based on the computational analysis of the gene expression changes, 3R4F (0.13 mg nicotine/L) elicited the highest biological impact (100%) in the context of Cell Fate, Cell Proliferation, Cell Stress, and Inflammatory Network Models at 4 h post-exposure. Whereas, the corresponding impact of THS2.2 (0.14 mg nicotine/L) was 7.6%.
2016-12-15 | E-MTAB-5318 | biostudies-arrayexpress
Project description:Cigarette smoke is a risk factor for inflammatory diseases, such as atherosclerosis. Tobacco smoke interacts with inflammatory cytokines to produce endothelial dysfunction and induces pro-inflammatory and pro-atherosclerotic effects in vascular tissue. Smooth muscle cells (SMCs) are present in the media of human arteries, and are considered protective against atherosclerotic plaque destabilization. Contractile SMCs are the most prominent cell type in the healthy vessel wall. SMCs are not terminally differentiated, and retain the ability to undergo a phenotypic switch from a contractile to a dedifferentiated synthetic state to express inflammatory markers and a phagocytic activity in response to environmental cues. The aim of our study was to evaluate the effects in human SMCs of lipophilic component from cigarette smoke condensate (CSC) and of hydrophilic components of Electronic-cigarette, Tobacco heating products, or cigarette smoke.
2023-05-10 | PXD041174 | Pride