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Control of breast cancer cell migration by a p63-regulated signaling network (RNA)

ABSTRACT: Through analysis of a high-content screen we discovered that mir-203 can impair cell migration by suppressing p63 expression. We further determined that p63 promotes motility by inducing the expression of multiple target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62568 | GEO | 2014/10/22

SECONDARY ACCESSION(S): PRJNA264426

REPOSITORIES: GEO

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Control of breast cancer cell migration by a p63-regulated signaling network (RNA)

Project description:Through analysis of a high-content screen we discovered that mir-203 can impair cell migration by suppressing p63 expression. We further determined that p63 promotes motility by inducing the expression of multiple target genes. Total RNA isolated from cell lines with different rated of motility was compared.

2014-10-22 | E-GEOD-62568 | biostudies-arrayexpress

Control of breast cancer cell migration by a p63-regulated signaling network (miRNA)

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siRNA profiling of human keratinocyte and squamous cell carcinoma cell lines knocked down with p63 reveals loss of p63 leads to increased cell migration and up-regulation of genes involved in invasion and metastasis

Project description:p63, a homologue of the tumor suppressor p53, is critical for the development and maintenance of squamous epithelia. p63 is specifically expressed in the basal layers of stratified epithelial tissues and is considered a specific marker for cells of this type. The role of p63 in tumorigenesis remains poorly defined. Numerous studies have highlighted the oncogenic potential of the predominant p63 isoform DeltaNp63alpha; however, data suggest that other p63 proteins can act as tumor suppressors or alter the metastatic potential of tumors. DeltaNp63alpha can act as a transcriptional repressor, but the link between the transcriptional functions of p63 and its biological role is still unclear. In this study, we used a loss-of-function approach to investigate the transcriptional programs controlled by p63. Disruption of p63 in squamous cell lines resulted in down-regulation of transcripts specifically expressed in squamous tissues and a significant alteration of keratinocyte differentiation. Interestingly, we found that disruption of p63 led to up-regulation of markers of nonepithelial tissues (mesenchyme and neural tissue) in both primary and immortalized squamous cells. Many of these up-regulated genes are associated with increased capacity for invasion and metastasis in tumors. Furthermore, loss of p63 expression was accompanied by a shift toward mesenchymal morphology and an increase in motility in primary keratinocytes and squamous cell lines. We conclude that loss of endogenous p63 expression results in up-regulation of genes associated with invasion and metastasis, and predisposes to a loss of epithelial and acquisition of mesenchymal characteristics. These findings have implications for the role of p63 in both development and tumorigenesis.

2007-11-11 | E-GEOD-4975 | biostudies-arrayexpress

Control of breast cancer cell migration by a p63-regulated signaling network (RNA)

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Transcription profiling of skin from p63 null and wild type mice to identify genes that are directly or indirectly regulated by p63.

Project description:In the absence of p63 expression, the epidermis fails to commit to stratification, resulting in aborted skin development. In this study, gene expression profiles of E18.5 p63 null and wt skin, were compared in an effort to identify genes that are directly or indirectly regulated by p63. Experiment Overall Design: E18.5 embryos were obtained from matings between p63 heterozygous mice. RNA was isolated from the skin of two p63 null and two wild type embryos.

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p63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

Project description:Analysis of P63-regulated genes at gene expression level. The hypothesis tested in the present study was that P63 regulates specific epithelial-to-mesenchymal transition states in breast cancer cells.

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Control of breast cancer cell migration by a p63-regulated signaling network

Project description:This SuperSeries is composed of the SubSeries listed below.

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Chromatin modification is not a prerequisite for p63 binding but p63 binding can elicit chromatin remodeling

Project description:Transcription factor (TF) p63 is a master regulator playing critical roles in epidermal development and other cellular processes. Our lab’s previous research deciphered a distinct chromatin architecture at p63 bound site in keratinocytes. In order to figure out whether those chromatin modifications already exist before p63 binding, or p63 occupancy contributes to such chromatin marks, we built p63-expressing cell lines. We then obtained p63 bound regions in these overexpressing cell line, and looked at different histone marks at those sites before p63 occupancy. As shown in the results, before p63 binding, the targeting sites have barely detectable histone marks, indicating p63’s capability to approach unmodified chromatins. Moreover, there is no significant difference in chromatin marks between p63 bound sites and unbound sites when no p63 binding happens. Our in vivo findings were confirmed by examining p63 binding to unmodified nucleosomes in vitro, showing that histone modification is not indispensable for p63 binding but binding site positioning on nucleosome does play a role. Overall, our results suggest that histone modifications do not affect p63 binding, and p63 protein can bind to inaccessible, weakly modified chromatin regions in vivo.

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Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines

2016-08-11 | E-GEOD-72009 | biostudies-arrayexpress

ChIP-seq of p63 and RNA-seq of knockdown and overexpression of p63

Project description:We performed ChIP-seq of p63 in ME-180 cell line and RNA-seq of knockdown and overexpression of p63

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