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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

Module detection via dynamic tree cutting (WGCNA output). Each vertical line a.k.a. “leaf” represents a gene. A group of leaves form a “branch” which is densely interconnected co-expressing genes. Multiple branches converge into a tree which corresponds to a module. A random color is assigned to a module (i.e. turquoise and brown are shown here). Heatmaps show expression level of genes from corresponding experimental group (shown on left with starting with “cor.”) and denoted module (shown by “Module colors”). Heatmaps: Red — positive, green — negative.
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f0030: Module detection via dynamic tree cutting (WGCNA output). Each vertical line a.k.a. “leaf” represents a gene. A group of leaves form a “branch” which is densely interconnected co-expressing genes. Multiple branches converge into a tree which corresponds to a module. A random color is assigned to a module (i.e. turquoise and brown are shown here). Heatmaps show expression level of genes from corresponding experimental group (shown on left with starting with “cor.”) and denoted module (shown by “Module colors”). Heatmaps: Red — positive, green — negative.

Mentions: Once the Soft threshold power beta value was chosen based on the criterion of approximate scale-free topology, we turned the adjacencies into Topological Overlap Matrix (TOM). The main objective of our study was to identify changes in biological function and pathway of normal oral keratinocytes due to EtOH and/or nicotine. Although it is possible to simply rank microarray expression data based on the fold change alone, the strength of WGCNA comes from its robustness and sensitivity to identify genes/proteins of interest and its ability to cluster genes of interest into a module based on their interconnectedness [4]. We set merging threshold value at 0.25, beta power value at 9, maximum block size at 10,000 and minimum module size at 1000. The rest of the “blockwiseModules” function was left at its default values. The result from automatic module detection via dynamic tree cutting is shown in Fig. 6.


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)

Module detection via dynamic tree cutting (WGCNA output). Each vertical line a.k.a. “leaf” represents a gene. A group of leaves form a “branch” which is densely interconnected co-expressing genes. Multiple branches converge into a tree which corresponds to a module. A random color is assigned to a module (i.e. turquoise and brown are shown here). Heatmaps show expression level of genes from corresponding experimental group (shown on left with starting with “cor.”) and denoted module (shown by “Module colors”). Heatmaps: Red — positive, green — negative.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0030: Module detection via dynamic tree cutting (WGCNA output). Each vertical line a.k.a. “leaf” represents a gene. A group of leaves form a “branch” which is densely interconnected co-expressing genes. Multiple branches converge into a tree which corresponds to a module. A random color is assigned to a module (i.e. turquoise and brown are shown here). Heatmaps show expression level of genes from corresponding experimental group (shown on left with starting with “cor.”) and denoted module (shown by “Module colors”). Heatmaps: Red — positive, green — negative.
Mentions: Once the Soft threshold power beta value was chosen based on the criterion of approximate scale-free topology, we turned the adjacencies into Topological Overlap Matrix (TOM). The main objective of our study was to identify changes in biological function and pathway of normal oral keratinocytes due to EtOH and/or nicotine. Although it is possible to simply rank microarray expression data based on the fold change alone, the strength of WGCNA comes from its robustness and sensitivity to identify genes/proteins of interest and its ability to cluster genes of interest into a module based on their interconnectedness [4]. We set merging threshold value at 0.25, beta power value at 9, maximum block size at 10,000 and minimum module size at 1000. The rest of the “blockwiseModules” function was left at its default values. The result from automatic module detection via dynamic tree cutting is shown in Fig. 6.

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