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Gene expression signatures affected by ethanol and/or nicotine in normal human normal oral keratinocytes (NHOKs).

Kim JJ, Khalid O, Duan L, Kim R, Elashoff D, Kim Y - Genom Data (2014)

Bottom Line: We hypothesized that nicotine/alcohol induces deregulation of epigenetic machinery and leads to epigenetic alterations, which subsequently affect transcriptional regulation in oral epithelial stem cells.As an initiating step we have profiled transcriptomic alterations induced by combinatory administration of EtOH and nicotine in primary normal human oral keratinocytes.Our data provide comprehensive transcriptomic map describing molecular changes induced by EtOH and nicotine on normal human oral keratinocytes.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Stem Cell and Cancer Epigenetic Research, UCLA School of Dentistry, Los Angeles, CA, USA.

ABSTRACT
It has been reported that nicotine/alcohol alter epigenetic control and lead to abrogated DNA methylation and histone modifications, which could subsequently perturb transcriptional regulation critically important in cellular transformation. The aim of this study is to determine the molecular mechanisms of nicotine/alcohol-induced epigenetic alterations and their mechanistic roles in transcriptional regulation in human adult stem cells. We hypothesized that nicotine/alcohol induces deregulation of epigenetic machinery and leads to epigenetic alterations, which subsequently affect transcriptional regulation in oral epithelial stem cells. As an initiating step we have profiled transcriptomic alterations induced by combinatory administration of EtOH and nicotine in primary normal human oral keratinocytes. Here we provide detailed experimental methods, analysis and information associated with our data deposited into Gene Expression Omnibus (GEO) under GSE57634. Our data provide comprehensive transcriptomic map describing molecular changes induced by EtOH and nicotine on normal human oral keratinocytes.

No MeSH data available.


Related in: MedlinePlus

Threshold beta value calculation (WGCNA output). The left panel shows the Scale-Free Topology (SFT) Index in y-axis as a function of the Soft Threshold in x-axis. The graph is reaching a saturation point at threshold beta value = 9. The right panel shows the Mean Connectivity in y-axis as a function of the Soft Threshold in x-axis. The slope of the regression line should be close to − 1.
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f0025: Threshold beta value calculation (WGCNA output). The left panel shows the Scale-Free Topology (SFT) Index in y-axis as a function of the Soft Threshold in x-axis. The graph is reaching a saturation point at threshold beta value = 9. The right panel shows the Mean Connectivity in y-axis as a function of the Soft Threshold in x-axis. The slope of the regression line should be close to − 1.

Mentions: The sample dendogram and trait heatmap allows the users to check the data for excessive missing values and visualize obvious outlier samples. Next, a soft threshold power beta value based on the scale free topology was calculated. This is a critical step since the success of subsequent network construction and identification of modules depends on choosing the most ideal soft threshold power beta value. WGCNA allows the users to choose an automated “convenient-1-step method” or more customizable step-by-step method. It is important to maximize scale-free topology model fit (R^2) while maintaining a high mean number of connections. Generally, R^2 should be close to 1, the mean connectivity should be high so that the network contains enough information. The slope of the regression line should be close to − 1. We chose the soft threshold power beta = 9 since this was where the curve reached a saturation point in the Soft Threshold (SFT) graph (Fig. 5).


Gene expression signatures affected by ethanol and/or nicotine in normal human normal oral keratinocytes (NHOKs).

Kim JJ, Khalid O, Duan L, Kim R, Elashoff D, Kim Y - Genom Data (2014)

Threshold beta value calculation (WGCNA output). The left panel shows the Scale-Free Topology (SFT) Index in y-axis as a function of the Soft Threshold in x-axis. The graph is reaching a saturation point at threshold beta value = 9. The right panel shows the Mean Connectivity in y-axis as a function of the Soft Threshold in x-axis. The slope of the regression line should be close to − 1.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4127651&req=5

f0025: Threshold beta value calculation (WGCNA output). The left panel shows the Scale-Free Topology (SFT) Index in y-axis as a function of the Soft Threshold in x-axis. The graph is reaching a saturation point at threshold beta value = 9. The right panel shows the Mean Connectivity in y-axis as a function of the Soft Threshold in x-axis. The slope of the regression line should be close to − 1.
Mentions: The sample dendogram and trait heatmap allows the users to check the data for excessive missing values and visualize obvious outlier samples. Next, a soft threshold power beta value based on the scale free topology was calculated. This is a critical step since the success of subsequent network construction and identification of modules depends on choosing the most ideal soft threshold power beta value. WGCNA allows the users to choose an automated “convenient-1-step method” or more customizable step-by-step method. It is important to maximize scale-free topology model fit (R^2) while maintaining a high mean number of connections. Generally, R^2 should be close to 1, the mean connectivity should be high so that the network contains enough information. The slope of the regression line should be close to − 1. We chose the soft threshold power beta = 9 since this was where the curve reached a saturation point in the Soft Threshold (SFT) graph (Fig. 5).

Bottom Line: We hypothesized that nicotine/alcohol induces deregulation of epigenetic machinery and leads to epigenetic alterations, which subsequently affect transcriptional regulation in oral epithelial stem cells.As an initiating step we have profiled transcriptomic alterations induced by combinatory administration of EtOH and nicotine in primary normal human oral keratinocytes.Our data provide comprehensive transcriptomic map describing molecular changes induced by EtOH and nicotine on normal human oral keratinocytes.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Stem Cell and Cancer Epigenetic Research, UCLA School of Dentistry, Los Angeles, CA, USA.

ABSTRACT
It has been reported that nicotine/alcohol alter epigenetic control and lead to abrogated DNA methylation and histone modifications, which could subsequently perturb transcriptional regulation critically important in cellular transformation. The aim of this study is to determine the molecular mechanisms of nicotine/alcohol-induced epigenetic alterations and their mechanistic roles in transcriptional regulation in human adult stem cells. We hypothesized that nicotine/alcohol induces deregulation of epigenetic machinery and leads to epigenetic alterations, which subsequently affect transcriptional regulation in oral epithelial stem cells. As an initiating step we have profiled transcriptomic alterations induced by combinatory administration of EtOH and nicotine in primary normal human oral keratinocytes. Here we provide detailed experimental methods, analysis and information associated with our data deposited into Gene Expression Omnibus (GEO) under GSE57634. Our data provide comprehensive transcriptomic map describing molecular changes induced by EtOH and nicotine on normal human oral keratinocytes.

No MeSH data available.


Related in: MedlinePlus