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DLX3-dependent p53 signaling network controls keratinocyte cell cycle and squamous tumor growth

ABSTRACT: DLX3-dependent p53 signaling network controls keratinocyte cell cycle and squamous tumor growth

PROVIDER: PRJNA280744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1959571.fastq.gz	Fastqsanger.gz
	SRR1959572.fastq.gz	Fastqsanger.gz
	SRR1959573.fastq.gz	Fastqsanger.gz
	SRR1959574.fastq.gz	Fastqsanger.gz
	SRR1959575.fastq.gz	Fastqsanger.gz

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Transcriptional changes in murine keratinocyte harbouring heterozygous or homozygous R245W p53 mutation in vitro

Project description:Human epidermis is colonized by clones carrying UV light induced p53 mutations, thought to be the origin of keratinocyte derived cancers, but the cellular mechanisms underlying the formation of these clones are not well understood. To address this we generated a new conditional knock-in mouse model bearing one of the hot spot mutations, R245W (R248W in human), targeted to the p53 locus, with its expression linked to a GFP reporter to enable lineage tracing. This mutation is one of the most frequently observed in cutaneous squamous cell carcinomas. We find that when induced in individual epidermal interfollicular progenitor cells the p53 mutant cells are dominant over wild type keratinocytes expanding to colonize the majority of the interfollicular epidermis. This process is accelerated by sub erythema doses ultraviolet light exposure. In vitro analysis of the trancriptomes can explain the intrinsic function driving clonal expansion.

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DLX3-dependent p53 signaling network controls keratinocyte cell cycle and squamous tumor growth

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

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Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.

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Expression profiling of cutaneous squamous cell carcinoma with perineural invasion implicates the p53 pathway in the process

Project description:Squamous cell carcinoma (SCC) is the second most common cancer worldwide and accounts for approximately 30% of all keratinocyte cancers. The vast majority of cutaneous SCCs of the head and neck (cSCCHN) are readily curable with surgery and/or radiotherapy unless high-risk features are present. Perineural invasion (PNI) is recognized as one of these high-risk features. The molecular changes during clinical PNI in cSCCHN have not been previously investigated. In this study, we assessed the global gene expression differences between cSCCHN with or without incidental or clinical PNI. The results of the analysis showed signatures of gene expression representative of activation of p53 in tumors with PNI compared to tumors without, amongst other alterations. Immunohistochemical staining of p53 showed cSCCHN with clinical PNI to be more likely to exhibit a diffuse over-expression pattern, with no tumors showing normal p53 staining. DNA sequencing of cSCCHN samples with clinical PNI showed no difference in mutation number or position with samples without PNI, however a significant difference was observed in regulators of p53 degradation, stability and activity. Our results therefore suggest that cSCCHN with clinical PNI may be more likely to contain alterations in the p53 pathway, compared to cSCCHN without PNI.

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