Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA120057 | ENA |
REPOSITORIES: ENA
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Project description:The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells.
2011-02-10 | GSE24414 | GEO
Project description:The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. 2 samples were included, a control passaged human oral immortal OKF6 cells and cigarette smoke extract-treated OKF6 cells. The chronic treatment for cigarette smoke extract is 7 months. Genomic DNAs were extracted from both cells and then used for Affymetix MitoChip Version 2.0 analysis.
2011-02-10 | E-GEOD-24414 | biostudies-arrayexpress
Project description:Effects of cigarette smoke on the human airway epithelial cell transcriptome
| PRJNA88045 | ENA
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:Besides its well-known effects increasing predisposition to oral cancer, cigarette smoke (CS) exposure is an important risk factor for many conditions including periodontal diseases, gingivitis and other benign mucosal disorders. Smoking cessation remains the most effective approach for minimizing risk of smoking-related diseases. However, reduction of harmful constituents by heating rather than combusting tobacco, without modifying the amount of nicotine, is a promising new paradigm in harm reduction. In this study we compared effects of exposure to aerosol derived from a candidate modified risk tobacco product, the tobacco heating system (THS) 2.2, with those of conventional smoke generated from the 3R4F reference cigarette. Human organotypic oral epithelial tissue cultures (EpiOralï¾, MatTek Corporation) were exposed for 28 min to 3R4F CS or THS2.2 aerosol, both diluted with air to comparable nicotine concentrations (0.32 or 0.51 mg nicotine/L aerosol/smoke for 3R4F and 0.31 or 0.46 mg/L for THS2.2). We also tested one higher concentration (1.09 mg/L) of THS2.2. A systems toxicology approach was employed combining cellular assays (i.e. cytotoxicity and cytochrome P450 activity assays), comprehensive molecular investigations of the buccal epithelial transcriptome (mRNA and miRNA) by means of computational network biology, measurements of secreted proinflammatory markers, histopathological analysis. We observed that the impact of 3R4F CS was greater than THS2.2 aerosol in terms of cytotoxicity, morphological tissue alterations and secretion of inflammatory mediators. Analysis of the transcriptomic changes in the exposed oral cultures revealed significant perturbations in various network models such as apoptosis, necroptosis, senescence, xenobiotic metabolism, oxidative stress and nuclear factor (erythroid-derived 2)-like 2 (NFE2L2) signaling. The stress responses following THS2.2 aerosol exposure were markedly decreased and the exposed cultures recovered better as compared with those exposed to 3R4F CS.
2016-07-26 | E-MTAB-4742 | biostudies-arrayexpress
Project description:Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells
| PRJNA132715 | ENA
Project description:Smoking is the leading cause of preventable death worldwide. It increases the risk for various diseases including respiratory diseases, vascular diseases and different cancers including lung, oral and bladder cancer. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon cigarette smoke exposure are yet to be fully elucidated. It is crucial to note that disease development is observed upon chronic exposure to cigarette smoke, as opposed to a short-term exposure. Hence, we sought to investigate the effect of chronic smoke exposure on normal oral keratinocytes (OKF6/TERT1). We employed tandem mass tag-based quantitative proteomic and phosphoproteomic approaches to investigate the proteomic and signaling changes in OKF6/TERT1 cells chronically exposed to cigarette smoke compared to untreated cells. LC/MS2 analysis resulted in the quantification of 5,067 proteins among which expression of 360 proteins were found to be dysregulated in at least one replicate. Phosphoproteomic analysis revealed quantification of 3,647 phosphopeptides corresponding to 1,801 proteins. Majority of the dysregulated proteins were seen to be involved in cellular processes such as cell growth, cellular communication and energy metabolism. This study will aid in elucidating the effects of smoking in oral cancer and in the identification of potential candidates molecules which could serve as early detection biomarkers or therapeutic targets.
2018-03-05 | PXD007637 | 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 smoking is the major cause of chronic inflammatory diseases such as Chronic Obstructive Pulmonary Disease (COPD). It is paramount to develop pharmacological interventions and delivery strategies against the cigarette smoke (CS) associated oxidative stress in COPD. This study in Wistar rats examined cysteamine in nanoemulsions to counteract the cigarette smoke distressed microenvironment. In vivo, 28 days of cigarette smoke and 15 days of cysteamine nanoemulsions treatment starting on 29th day consisting of oral and inhalation routes were established in Wistar rats. Additionally, we conducted inflammatory and epithelial-to-mesenchymal transition (EMT) studies in vitro in human bronchial epithelial cell lines (BEAS2B) using 5% cigarette smoke extract. Inflammatory and anti-inflammatory markers such as TNF-α, IL-6, IL-1ß, IL-8, IL-10, IL-13, have been quantified in bronchoalveolar lavage fluid (BALF) to evaluate the effects of the cysteamine nanoemulsions in normalizing the diseased condition. Histopathological analysis of the alveoli and the trachea showed the distorted, lung parenchyma and ciliated epithelial barrier, respectively. To obtain mechanistic insights into the cigarette smoke COPD rat model, “shotgun” proteomics of the lung tissues have been carried out using high-resolution mass spectrometry wherein genes such as ABI1, PPP3CA, PSMA2, FBLN5, ACTG1, CSNK2A1, and ECM1 exhibited significant differences across all the groups. Pathway analysis showed autophagy, signaling by receptor tyrosine kinase, cytokine signaling in immune system, extracellular matrix organization, and hemostasis, as the major contributing pathways across all the studied groups. This work offers new preclinical findings on how cysteamine taken orally or inhaled can combat cigarette smoke-induced oxidative stress.
2023-08-21 | PXD033529 | Pride
Project description:In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking.
2015-12-31 | GSE54861 | GEO