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Examining the transcriptional changes thar result from loss of p53 in mutant p53 A431 cells

ABSTRACT: Examining the transcriptional changes thar result from loss of p53 in mutant p53 A431 cells

PROVIDER: PRJNA1246068 | ENA |

REPOSITORIES: ENA

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Examining the transcriptional changes thar result from loss of p53 in mutant p53 A431 cells

Project description:A431 mutant p53 cells are able to engulf neighbouring cancer cells. Loss of p53 in these cells impairs this behaviour. To determine if transcriptional changes could underlie these phenotypic changes we compared A431 cells in which p53 was deleted using CRISPR (p53 KO) to parental cells (P) or cells that were transfected with a CRISP control construct (p53 ctr). Three indivicual clones were derived from single cells and compared to each other.

2025-07-09 | GSE293711 | GEO

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells No treatmentt, A431-P cells vs. A431-III cells. A431-P cells are used as a reference to invstigate A431-III cells.

2013-06-18 | E-GEOD-47996 | biostudies-arrayexpress

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells

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Expression data to parental A431 VS CD109 KO A431

Project description:Expression data to parental A431 VS CD109 KO A431

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Transcriptome profiling of RBM3 overexpression in A431 cells

Project description:This study aims to investigate the transcriptional changes induced by overexpression of RNA-binding protein RBM3 in A431 human epidermoid carcinoma cells. Lentiviral transduction was used to stably overexpress RBM3 in A431 cells. Total RNA was extracted from RBM3 overexpressing cells and control cells, followed by RNA-seq library preparation and sequencing on Illumina platform. Differential gene expression analysis will be performed to identify RBM3 targets and regulatory networks.

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The impact of P53 loss on transcriptome changes following loss of Apc in the intestine

Project description:BACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated. METHODS: We have conditionally deleted the Adenomatous Polyposis coli gene (Apc) from the adult murine intestine in wild type and p53 deficient environments and subsequently compared the phenotype and transcriptome profiles in both genotypes. RESULTS: Expression of p53 was shown to be elevated following the conditional deletion of Apc in the adult small intestine. Furthermore, p53 status was shown to impact on the transcription profile observed following Apc loss. A number of key Wnt pathway components and targets were altered in the p53 deficient environment. However, the aberrant phenotype observed following loss of Apc (rapid nuclear localisation of beta-catenin, increased levels of DNA damage, nuclear atypia, perturbed cell death, proliferation, differentiation and migration) was not significantly altered by the absence of p53. CONCLUSION: p53 related feedback mechanisms regulating Wnt signalling activity are present in the intestine, and become activated following loss of Apc. However, the physiological Wnt pathway regulation by p53 appears to be overwhelmed by Apc loss and consequently the activity of these regulatory mechanisms is not sufficient to modulate the immediate phenotypes seen following Apc loss. Thus we are able to provide an explanation to the apparent contradiction that, despite having a Wnt regulatory capacity, p53 loss is not associated with early lesion development. Samples were collected from genetically modified mice. Gene recombination was induced using IP administration of beta-napthoflavone.

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Mutant p53 interactome study with IP-MS

Project description:Inactivating TP53 mutations lead to a loss of function of p53, but can also often result in oncogenic gain-of-function (GOF) of mutant p53 (mutp53) proteins which promote tumor development and progression. The GOF activities of TP53 mutations are well documented, but the mechanisms involved remain poorly understood. Here, we study the mutp53 interactome with IP-MS.

2023-11-27 | PXD047094 | Pride

RNA-seq of TCF4 silencing in A431 cells

Project description:TCF4 was silenced in cutaneous squamous cell carcinoma of A431 cells, and detected the mRNA profiles compared to the negative control and blank control.

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RNA-seq of A431 cells expressing control or ARID1A-targeting shRNAs

Project description:We examined gene expression level in A431 cells expressing control or ARID1A-targeting shRNAs to study the mechanism underlying the tumor suppressive effect of ARID1A.

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p53 exon 11 mutants generated by CRISPR/Cas9 result in aberrant alternative splicing.

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