Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-13309
PROVIDER: PRJNA109891 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Polycomb-mediated repression of Dkk-1 activates Wnt signaling and enhances tumorigenic potential of lung cancer cells following tobacco smoke exposure Keywords: tobacco Smoke, lung cancer, epigenetics
2009-04-10 | GSE13309 | GEO
Project description:Polycomb-mediated repression of Dkk-1 activates Wnt signaling and enhances tumorigenic potential of lung cancer cells following tobacco smoke exposure Experiment Overall Design: microarray techniques were used to examine proliferation and gene expression in A549 and Calu-6 lung cancer cells cultured in normal media with or without tobacco smoke condensate (TSC)
2009-04-19 | E-GEOD-13309 | biostudies-arrayexpress
Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of lung toxicity in response to crystalline silica exposure. Nevertheless, the precise role of tobacco smoke exposure on the lung response to tobacco smoke exposure and the underlying mechanisms remain largely elusive. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary toxicity and the underlying molecular mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in rats exposed to air, crystalline silica, tobacco smoke, or crystalline silica plus tobacco smoke. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by tobacco smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to tobacco smoke, silica or a combination of both compared with the air exposed control rats.
2024-12-31 | GSE149286 | GEO
Project description:Our previous studies have shown that tobacco smoke exposure exacerbated the lung response to crystalline silica exposure in rats. The objective of the present study, a follow-up to our previous study, was to determine the effect of tobacco smoke exposure cessation on the lung response to crystalline silica exposure in the rats. Rats were exposed to air, crystalline silica (1 week followed by a 1 year progression/recovery period with no exposure), tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure), or crystalline silica (1 week) plus tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure). Lung toxicity was determined at the end of the 1-year progression/recovery period in all 4 groups of the rats. Silica exposure resulted in significant lung toxicity which was further exacerbated by tobacco smoke exposure in the rats. Cessation of cigarette smoke exposure did not result in reversal of the silica-induced lung toxicity despite exacerbation of the toxicity by tobacco smoke.
2024-12-31 | GSE155924 | GEO
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.
2011-02-02 | GSE19667 | GEO
Project description:Cigarette smoking is the leading cause of lung cancer worldwide. Carcinogens in smoke produced during the combustion of cigarette tobacco are responsible for airway epithelial changes underlying lung carcinogenesis. Reduction of harmful constituents by heating rather than combusting tobacco would be a sound strategy to reduce the risk for lung cancer. In this study we characterized the functional and molecular changes during long-term treatment of human bronchial epithelial cells with total particulate matter (TPM) from a new candidate modified risk tobacco product (cMRTP), the tobacco heated system 2.2 (THS2.2) in comparison with TPM from combustible 3R4F reference cigarettes.
2018-03-08 | E-MTAB-5697 | biostudies-arrayexpress
Project description:Cigarette smoking is the leading cause of lung cancer worldwide. Carcinogens in smoke produced during the combustion of cigarette tobacco are responsible for airway epithelial changes underlying lung carcinogenesis. Reduction of harmful constituents by heating rather than combusting tobacco would be a sound strategy to reduce the risk for lung cancer. In this study we characterized the functional and molecular changes during long-term treatment of human bronchial epithelial cells with total particulate matter (TPM) from a new candidate modified risk tobacco product (cMRTP), the tobacco heated system 2.2 (THS2.2) in comparison with TPM from combustible 3R4F reference cigarettes.
2018-03-08 | E-MTAB-6119 | biostudies-arrayexpress
Project description:MicroRNAs are critical mediators of stem cell pluripotency, differentiation and malignancy. Limited information exists regarding microRNA alterations that facilitate initiation and progression of human lung cancers. In this study, array techniques were used to evaluate microRNA expression in normal human respiratory epithelia and lung cancer cells cultured in the presence or absence of cigarette smoke condensate (CSC). Under relevant exposure conditions, CSC significantly repressed miR-487b in these cells. Subsequent experiments demonstrated that miR-487b directly targets SUZ12, BMI1, Wnt5a, c-Myc and K-ras. Repression of miR-487b correlated with over-expression of these targets in primary lung cancers, and coincided with DNA methylation, de-novo nucleosome occupancy, and decreased H2AZ and TCF1 levels within the miR-487b genomic locus. Deoxyazacytidine de-repressed miR-487b, and attenuated CSC-mediated silencing of miR-487b. TGF-β1 recapitulated CSC-mediated repression of miR-487b. Constitutive expression of miR-487b abrogated Wnt signaling; inhibited in-vitro proliferation and invasion of lung cancer cells mediated by CSC or over-expression of miR-487b targets, and decreased growth and metastatic potential of lung cancer cells in-vivo. Collectively, these findings indicate that miR-487b is a novel tumor suppressor microRNA silenced by epigenetic mechanisms during tobacco-induced pulmonary carcinogenesis, and suggest that DNA demethylating agents may be useful for activating miR-487b for lung cancer therapy.
2012-12-18 | GSE42962 | GEO
Project description:MicroRNAs are critical mediators of stem cell pluripotency, differentiation and malignancy. Limited information exists regarding microRNA alterations that facilitate initiation and progression of human lung cancers. In this study, array techniques were used to evaluate microRNA expression in normal human respiratory epithelia and lung cancer cells cultured in the presence or absence of cigarette smoke condensate (CSC). Under relevant exposure conditions, CSC significantly repressed miR-487b in these cells. Subsequent experiments demonstrated that miR-487b directly targets SUZ12, BMI1, Wnt5a, c-Myc and K-ras. Repression of miR-487b correlated with over-expression of these targets in primary lung cancers, and coincided with DNA methylation, de-novo nucleosome occupancy, and decreased H2AZ and TCF1 levels within the miR-487b genomic locus. Deoxyazacytidine de-repressed miR-487b, and attenuated CSC-mediated silencing of miR-487b. TGF-?1 recapitulated CSC-mediated repression of miR-487b. Constitutive expression of miR-487b abrogated Wnt signaling; inhibited in-vitro proliferation and invasion of lung cancer cells mediated by CSC or over-expression of miR-487b targets, and decreased growth and metastatic potential of lung cancer cells in-vivo. Collectively, these findings indicate that miR-487b is a novel tumor suppressor microRNA silenced by epigenetic mechanisms during tobacco-induced pulmonary carcinogenesis, and suggest that DNA demethylating agents may be useful for activating miR-487b for lung cancer therapy. MicroRNA PCR array analysis. Human RT2 miRNA PCR Arrays (MAH-3100E-12) were obtained from SA Biosciences. Two hundred ng of isolated miRNA was used for reverse transcription and the entire first strand cDNA was diluted and distributed amongst the 384 wells of the super-array plate. The reactions were performed with RT² SYBR Green / ROX PCR Master Mix (SABiosciences). Results were analyzed using software provided by the vendor (http://www.sabiosciences.com/pcr/arrayanalysis.php).
2012-12-18 | E-GEOD-42962 | biostudies-arrayexpress
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