Molecular effects of EtOH and Nicotine on normal human oral keratinocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57634 | GEO | 2014/05/14
SECONDARY ACCESSION(S): PRJNA247378
REPOSITORIES: GEO
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Project description:We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis. Primary normal human oral keratinocytes were cultured and treated with various dose of EtOH (0, 20 and 50 mM) and cotreated with various dose of nicotine (0, 0.5 and 1uM) for 24 hours. Total RNA was isolated and subjected to gene expression microarray analysis using Affymetrix Human Genome 2.0 plus.
2014-05-14 | E-GEOD-57634 | biostudies-arrayexpress
Project description:we found that chronic oral (3 months) administration of nicotine had different effects on transcriptomic profiling in prefrontal forebrain cortex of wildtype (WT) and Presenilin 1/2 double knockout mice.
2024-01-01 | GSE211983 | GEO
Project description:This was a hypothesis generating experiment to look at miR expression in a range of oral keratinocytes, including normal, precancer and oral cancer samples. The cells were cultures as per standard protocols (duplicate cultures) before assessment on the Affy miRNA array (1.0) one normal oral keratinocyte, one precancer, and 2 cancer samples, all in duplicate
2013-11-28 | E-GEOD-52811 | biostudies-arrayexpress
Project description:The in utero environment is a critical determinant of the immediate and future health of the developing fetus. Two of the most commonly used drugs during pregnancy are alcohol and nicotine. While prolonged gestational exposure to alcohol or nicotine has been associated with a range of adverse outcomes in the offspring, the consequences of exposure during early gestation only are less well understood. Here, we use mouse models of relatively moderate early gestational ethanol or nicotine exposure to profile gene expression in whole male embryos at 9.5 days post coitum using an Illumina microarray.
2021-08-18 | GSE94347 | GEO
Project description:This was a hypothesis generating experiment to look at miR expression in a range of oral keratinocytes, including normal, precancer and oral cancer samples. The cells were cultures as per standard protocols (duplicate cultures) before assessment on the Affy miRNA array (1.0)
2013-11-28 | GSE52811 | GEO
Project description:Molecular effects of EtOH and Nicotine on normal human oral keratinocytes
| PRJNA247378 | ENA
Project description:Alcohol (ethanol, EtOH) consumption during pregnancy can result in fetal alcohol spectrum disorders (FASDs), which are characterized by prenatal and postnatal growth restriction and craniofacial dysmorphology. The specific mechanisms by which alcohol mediates these injuries have yet to be determined. Cell-derived extracellular vesicles, including exosomes and microvesicles containing several species of RNAs (exRNAs), have recently emerged as a mechanism of cell-to-cell communication. However, EtOH’s effects on the biogenesis and function of non-coding exRNAs during fetal development have not been explored. Therefore, we studied the effects of maternal EtOH exposure on the composition of exRNAs in the amniotic fluid (AF) using a rat fetal alcohol exposure (FAE) model. Timed pregnant Sprague Dawley rats received 0 or 2.5 g/kg of 20% EtOH by oral gavage on embryonic days 5, 8, 10, 12 and 15. Through RNA-Seq analysis we identified and verified AF exosomal miRNAs with differential expression levels specifically associated with maternal EtOH exposure.
2019-06-11 | GSE132437 | GEO
Project description:Shisha smoking is widely believed to be a hazard-free habit. Studies have reported shisha smoking to be associated with oral lesions as well ascarcinomas of the lung, esophagus, bladder, and pancreas. A better understanding of the underlying mechanism may contribute to the identification of biomarkers for targeted therapy and better prognosis of the disease. In this study, we have established a chronic model of shisha-exposed oral keratinocytes to study the effect of shisha smoking on oral cells. Normal oral keratinocytes (non-transformed and immortalised), OKF/TERT1, were chronically treated with shisha extract for 8 months. In vitro cellular assays as well as total proteomic analysis were performed using the OKF6/TERT1-Parental and shisha-exposed cells (OKF6/TERT1-Shisha) to understand the effect of shisha smoking on cellular transformation. Chronic exposure of OKF6/TERT1 cells with shisha resulted in a significant increase in cellular proliferation and cell invasion compared to the OKF6/TERT1-Parental cells. Quantitative proteomic analysis of OKF6/TERT1-Parental and OKF6/TERT1-Shisha cells resulted in the identification of more than 5,515 proteins. Of these 5,515 proteins, 82, 77, 106, 110 proteins were found to be differentially expressed (1.5-fold) in OKF6/TERT1 cells chronically treated with shisha extract for 2M, 4M, 6M and 8M, respectively when compared with OKF6/TERT1-Parental. Pathway and gene ontology-based analysis revealed dysregulation of interferon pathway, upregulation of proteins involved in cell growth and downregulation of immune processes. This study reveals that chronic treatment of normal oral keratinocytes with shisha leads to cellular transformation. Elucidation of dysregulated proteins in shisha smoke-exposed cells will provide insights into the effect of shisha smoking on oral cells and aid in identification of therapeutic targets.
2019-02-21 | PXD011106 | Pride
Project description:Tobacco use and alcohol consumption are two major contributing factors for head and neck squamous cell carcinoma (HNSCC) carcinogenesis. We combined the 4-nitroquinoline-1-oxide (4-NQO) oral carcinogenesis mouse model and the Meadows-Cook alcohol mouse models and performed next generation genome-wide RNA-sequencing of tongues. We determined changes in transcript levels in four groups: 4-NQO followed by ethanol treatment (4-NQO/EtOH), 4-NQO followed by normal drinking water (4-NQO/Untr.), vehicle control followed by ethanol treatment (V.C./EtOH), and vehicle control followed by normal drinking water (V.C./Untr.). We found that the 494 gene transcripts were significantly changed (at least a 2-fold change where p<0.05) in the V.C./EtOH group compared to the V.C./Untr. group. The 4-NQO/Untr. group had 1,808 transcripts significantly changed compared to the V.C./Untr group, while the 4-NQO/EtOH group had 3,606 significantly changed transcripts as compared to the V.C/Untr. group. This study is the first to show that 4-NQO followed by ethanol cause the largest number of changes in transcript levels in the tongue.
2015-10-06 | GSE62125 | GEO
Project description:Shisha smoking has been epidemiologically linked to development of oral lesions as well as various cancers. However, few molecular studies investigate the pathobiology of shisha induced cancer. In this study we investigate the effects of chronic shisha exposure in an in vitro model using normal, immortalized, non-transformed oral keratinocytes. Quantitative proteomic and phosphoproteomic analyses were performed on OKF6/TERT1 cells exposed to shisha for a period of 8 months. Gene Ontology and pathway analysis of dysregulated proteins and phosphoproteins were carried out to identify significantly enriched biological processes and pathways in shisha exposed cells compared to parental cells. Chronic shisha exposure resulted in increased cell scattering phenomenon in OKF6/TERT1 cells. Quantitative data analysis revealed differential phosphorylation of 164 phosphopeptides (fold change ≥1.5, p≤0.05) corresponding to 136 proteins. Kinases such as PRKCD were seen to be hyperphosphorylated. Pathway analysis revealed an enrichment of hyperphosphorylated and/or overexpressed proteins involved in the mTORC1 and EIF4F complexes. These complexes are associated with initiation of protein translation and are known to the affected in cancers. Network analysis also highlighted a downregulation of proteins associated with Type I interferon signaling in shisha exposed cells. High throughput phosphoproteomic analysis revealed global perturbations to the molecular milieu of oral keratinocytes upon shisha exposure. Further studies are needed to validate putative targets in oral cancer patients with shisha smoking history.
2019-07-23 | PXD011318 | Pride