Dataset Information

Transcriptional profiling of SNAI2 regulated genes in primary human keratinocytes.

ABSTRACT: Epithelial to mesenchymal transition transcription factors (EMT-TFs) such as SNAI2 have been found to be expressed endogenously in epidermal stem and progenitor cells and downregulated upon differentiation. The presence of SNAI2 in progenitor cells is necessary to repress the expression of differentiation genes by binding directly to their promoters. SNAI2 is downregulated upon differentiation which allows expression of differentiation genes. Furthermore overexpression of SNAI2 can block the differentiation process suggesting that the levels of SNAI2 are crucial to epidermal cell fate decisions. To address on a genome wide level the genes that are impacted by changing the levels of SNAI2, we performed microarray analysis on SNAI2 knockdown and overexpressing epidermal progenitor cells. Here we provide a detailed methods and analysis on these microarray data which has been deposited in Gene Expression Omnibus (GEO): GSE55269.

SUBMITTER: Mistry DS

PROVIDER: S-EPMC4360913 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Transcriptional profiling of SNAI2 regulated genes in primary human keratinocytes.

Mistry Devendra S DS Chen Yifang Y Wang Ying Y Sen George L GL

Genomics data 20150601

Epithelial to mesenchymal transition transcription factors (EMT-TFs) such as SNAI2 have been found to be expressed endogenously in epidermal stem and progenitor cells and downregulated upon differentiation. The presence of SNAI2 in progenitor cells is necessary to repress the expression of differentiation genes by binding directly to their promoters. SNAI2 is downregulated upon differentiation which allows expression of differentiation genes. Furthermore overexpression of SNAI2 can block the dif ...[more]

PMID: 25793155

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Project description:Our goal is to find new genes regulated by p21 in human primary cells . To get it we carried out a gene expression profiling in two different models, human myeloid leukemia K562 cells and human keratinocytes both of them with conditional expression of p21. In order to identify genes specifically modulated by p21 we compared with the cell line with overexpression of p27, because p21 and p27 belong to the same gene family and regulated the same genes specially in cell cycle. So, our intention is to identify only genes regulated by p21 and not p27. In order to confirm these results we studied the p21-dependent repression of mitotic genes in a different cellular system. We chose human primary keratinocytes because they are non-tumorigenic, non-immortalized and epithelial cells, in contrast to human myeloid leukemia K562 cells. Human primary keratinocytes were infected with recombinant adenoviruses expressing the full-length p21 protein. A dramatic increase in p21 in infected keratinocytes was demonstrated by RT-qPCR (as we show in the manuscript). As controls, we also infected the keratinocytes with adenovirus carrying the genes for p27 which overexpression was also confirmed by RT-qPCR (as we show in the manuscript). We prepared RNA 24 h after infection and performed large-scale expression assay using the Afftymetrix platform. The clustering analysis revealed that p21 provoked the down-regulation of a number genes involved in cell cycle control not shared by cells expressing p27 (as we show in the manuscript). Our goal, has been getting genes regulated more strongly by p21 and not by p27 in cell cycle and mitosis. Our result are supported because we have found the same genes in two different models and also we have validated (by RT-qPCR) more than 20 cell cycle and mitotic genes, found in our affymetrix arrays. Also we have found the region of p21 that is sufficient for gene regulation and for one gene we have described as p21 bind to the promoter. Finally, we have discussed in our manuscript how p21 can do this regulation by bioinformatic analysis of p21-target genes. The success of this study is to describe a new role of p21 as a transcriptional co-repressor in some systems.

Dataset Information

Transcriptional profiling of SNAI2 regulated genes in primary human keratinocytes.

Publications

Transcriptional profiling of SNAI2 regulated genes in primary human keratinocytes.

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