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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

ABSTRACT: Our goal was to assess transcriptional changes of the colon carcinoma cell line HCT116 TP53-/- in response to expression of the TP63 isoforms deltaNp63alpha or deltaNp63beta. The goal was to understand how these C-terminal isoforms of p63 might differentially regulate gene expression. We also assessed how differential binding of these isoforms and how they affect local changes in H3K27ac.

ORGANISM(S): Homo sapiens

PROVIDER: GSE283359 | GEO | 2024/12/13

REPOSITORIES: GEO

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Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

Project description:We analyzed the transcriptome changes of the colon carcinoma cell line HCT116 TP53-/- in response to expression of the TP63 isoforms deltaNp63alpha or deltaNp63beta. The goal was to understand how these C-terminal isoforms of p63 might differentially regulate gene expression.

2024-12-13 | GSE283357 | GEO

Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

Project description:Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta using ChIPseq of p63 and H3K27ac

| PRJNA1193516 | ENA

Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

Project description:Analysis of gene regulation by the TP63 isoforms deltaNp63alpha and deltaNp63beta

| PRJNA1193517 | ENA

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

Identification of HTRA4 as a trasncritpional target of P63 in trophoblast

Project description:The placenta plays a crucial role in pregnancy success. deltaNp63alpha (p63), a transcription factor from the TP53 family, is highly expressed in villous cytotrophoblasts (CTBs), the epithelial stem cells of the human placenta, and has been shown to be involved in CTB maintenance and differentiation. In this study, we set out to identify mechanism(s) of action of p63, by identifying its downstream targets. We evaluate gene expression changes following overexpression and knockdown of p63 in the JEG3 choriocarcinoma cell line, using microarray-based RNA profiling. We identify High temperature requirement A4 (HTRA4), a placenta-specific serine protease involved in trophoblast differentiation and altered in preeclampsia, as a gene reciprocally regulated by p63, and characterize its expression in primary human placental tissues by RNAseq (PMID 34540826; GSE173372) and in situ hybridization. Forced overexpression of deltaNp63alpha in JEG-3 was obtained by pCMV lentiviral vector infection (empty vector used as control). ) The pLKO.1-based non-targeting scramble and p63-specific short hairpin (shRNA) lentiviral plasmids were used for gene knock-down. Vectors were previously described in Li et al Am J Pathol. 2014 PMID: 25307348.

2024-03-27 | GSE251742 | GEO

FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

Project description:This study was designed to examine the requirement for the p63 transcription factor in Squamous Cell Carcinoma (SCC) tumor maintenance in an in vivo murine system. A tamoxifen-inducible Keratin 14-driven Cre recombinase transgene was used to conditionally excise p63 in advanced murine SCC tumors. These data show the context-dependent regulation of p63 target genes in cancer. Total RNA from murine Squamous Cell Carcinoma tumors was examined 1-3 days following genomic excision of TP63 in Keratin 14-expressing tumor cells.

2013-08-06 | E-GEOD-45929 | biostudies-arrayexpress

Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [ChIP-Seq]

Project description:In response to genotoxic stress the TP53 tumour suppressor activates target gene expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage. These canonical activities can be repressed by TP63 in normal stratifying epithelia to maintain proliferative capacity or drive proliferation of squamous cell carcinomas, where TP63 is frequently overexpressed/amplified. Here we use ChIP-sequencing, integrated with microarray analysis, to define the genome wide interplay between TP53 and TP63 in response to genotoxic stress in normal cells. We reveal that TP53 and TP63 bind to overlapping, but distinct cistromes of sites through utilization of distinctive consensus motifs and that TP53 is constitutively bound to a number of sites. We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity. Collectively, this results in a global TP53 dependent repression of cell cycle progression, mitosis and DNA damage repair concomitant with activation of anti-proliferative and pro-apoptotic canonical target genes. Further analyses reveals that in the absence of genotoxic stress TP63 plays an important role in maintaining expression of DNA repair genes, loss of which results in defective repair Examination of p63 and p53 binding sites in neonatal foreskin keratinocytes in response to adriamycin or cisplatin treatment

2014-04-11 | E-GEOD-56674 | biostudies-arrayexpress

Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [Affymetrix]

Project description:In response to genotoxic stress the TP53 tumour suppressor activates target gene expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage. These canonical activities can be repressed by TP63 in normal stratifying epithelia to maintain proliferative capacity or drive proliferation of squamous cell carcinomas, where TP63 is frequently overexpressed/amplified. Here we use ChIP-sequencing, integrated with microarray analysis, to define the genome wide interplay between TP53 and TP63 in response to genotoxic stress in normal cells. We reveal that TP53 and TP63 bind to overlapping, but distinct cistromes of sites through utilization of distinctive consensus motifs and that TP53 is constitutively bound to a number of sites. We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity. Collectively, this results in a global TP53 dependent repression of cell cycle progression, mitosis and DNA damage repair concomitant with activation of anti-proliferative and pro-apoptotic canonical target genes. Further analyses reveals that in the absence of genotoxic stress TP63 plays an important role in maintaining expression of DNA repair genes, loss of which results in defective repair Examination of gene expression levels of HFKS siRNA depleted for p53 or p63 in response to adriamycin or cisplatin treatment We analyzed RNA using the Affymetrix Human Exon 1.0 ST platform. Array data was processed using the AltAnalyze.

2014-04-30 | E-GEOD-57187 | biostudies-arrayexpress

Gene expression profiles induced by knockdown and overexpression of p63 variants in MCF-10A mammary epithelial cell line

Project description:p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. The p63 transactivating (TA) isoforms contain an amino-terminal exon that encodes a p53-like transactivation domain, whereas ÎN-isoforms lack this domain but contain the common DNA binding domain (DBD), suggesting that TAp63 and ÎNp63 isoforms may have opposing functions. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63Î³ or ÎNp63Î± isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis. Total RNA was isolated 48 h after retroviral or adenoviral infection and was subjected to reverse transcription, labelling and hybridization. The knockdown samples were performed in duplicate with shRNA vector control, shRNA targetting all isoforms of p63 (shDBD) and shRNA targetting p63 isoforms containing the transactivating (TA) domains. The overexpression samples were performed in triplicate with vector control, overexpression of the ÎNp63Î± isoform, and overexpression of the TAp63Î³ isoforms.

2010-03-23 | E-GEOD-20286 | biostudies-arrayexpress

mRNA expression profiling of p63-depleted versus wildtype ME180 cells

Project description:We investigated the transcriptional effects of p63 binding by analyzing ME180 cells depleted for all p63 isoforms via expression of a small hairpin RNA (shRNA) targeting the p63 oligomerization domain. Keywords: differential expression profiling from transcription factor depletion

2006-12-01 | GSE5993 | GEO

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