E-GEOD-13309
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA109891
PROVIDER: E-GEOD-13309 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-13309-analysis-methods.tsv | Tabular | |||
| E-GEOD-13309-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-13309-configuration.xml | Xml | |||
| E-GEOD-13309-percentile-ranks.tsv | Tabular | |||
| E-GEOD-13309.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 148 |
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Project description:Cigarette smoke is the most relevant risk factor for the development of lung cancer and chronic obstructive pulmonary disease. Many of its more than 4500 chemicals are highly reactive, thereby altering protein structure and function. Here, we used subcellular fractionation coupled to label-free quantitative MS to globally assess alterations in the proteome of different compartments of lung epithelial cells upon exposure to cigarette smoke extract. Proteomic profiling of the human alveolar derived cell line A549 revealed the most pronounced changes within the cellular secretome with preferential downregulation of proteins involved in wound healing and extracellular matrix organization. In particular, secretion of secreted protein acidic and rich in cysteine, a matricellular protein that functions in tissue response to injury, was consistently diminished by cigarette smoke extract in various pulmonary epithelial cell lines and primary cells of human and mouse origin as well as in mouse ex vivo lung tissue cultures. Our study reveals a previously unrecognized acute response of lung epithelial cells to cigarette smoke that includes altered secretion of proteins involved in extracellular matrix organization and wound healing. This may contribute to sustained alterations in tissue remodeling as observed in lung cancer and chronic obstructive pulmonary disease.
2019-01-08 | PXD007180 | Pride
Project description:Epidemiological data clearly establishes cigarette smoking as one of the major cause for lung cancer worldwide. There is no standard screening method for lung cancer even in high-risk populations and the overall five-year survival has not changed significantly in the last decade. First-line treatment for lung cancer includes surgical resection, chemotherapy, and radiation. Recently with the advancement of systems biology, targeted therapy has become one of the most preferred modes of treatment for cancer. Though certain targeted therapies such as anti-EGFR are in clinical practice, they have shown limited success in the smokers suffering from lung cancer. This demands the discovery of alternative drug targets through systematic investigation of altered signaling mechanisms. To study dysregulated signaling pathways due to chronic cigarette smzoke exposure, we carried out SILAC-based phosphoproteome analysis of lung cell line H358 chronically exposed to cigarette smoke. We identified 1,812 phosphosites, of which 278 were hyperphosphorylated (≥ 3-fold) in the H358 cells exposed to cigarette smoke. We identified several known and some novel kinases and key signaling molecules that were hyperphosphorylated in response to chronic exposure to cigarette smoke
2016-12-14 | PXD003108 | Pride
Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array
2012-04-01 | GSE36568 | GEO
Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.
2022-03-02 | PXD007108 | Pride
Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).
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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:Cigarette smoke has been associated with the development of various lung diseases including cancer. Dysregulation of miRNAs is known to affect protein expression which leads to diverse functional consequences. Investigating miRNA and protein expression in response to cigarette smoke exposure can lead to the identification of potential therapeutic and chemopreventive targets. We employed a SILAC-based quantitative proteomic analysis to identify proteins differentially expressed in response to cigarette smoke in H292 lung cancer cells. LC-MS/MS analysis led to the identification of 3,959 proteins, of which, 303 proteins were overexpressed and 112 proteins were found to be downregulated in cigarette smoke-treated H292 cells.
2018-10-25 | PXD003086 | Pride
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:Despite the fact that smoking is the major cause of lung cancer, there is no clear mechanism detailing how chronic exposure of cigarette smoke alters the global signaling in lung cells. To investigate the altered signaling in lung cells, in this study, we carried out SILAC-based quantitative phosphoproteomic analysis of H292 cells chronically exposed to cigarette smoke. Using high resolution Orbitrap Velos mass spectrometer, we identified hyperphosphorylation of 493 sites which corresponds to 341 proteins and 195 hypophosphorylated sites mapping to 142 proteins, upon smoke exposure (2.0-fold). Bioinformatics analysis revealed differentially phosphotylated proteins were involved in multiple cellular processes including cellular polarity, cytoskeletal remodelling, cellular migration, protein synthesis, autophagy and apoptosis. The present study will significantly improve the current knowledge of smoke mediated signaling in lung cells, which in turn may aid in the development of targeted therapies specially for smokers.
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