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RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

ABSTRACT: RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

PROVIDER: PRJEB42053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5000370.fastq.gz	Fastqsanger.gz
	ERR5000371.fastq.gz	Fastqsanger.gz
	ERR5000372.fastq.gz	Fastqsanger.gz
	ERR5000373.fastq.gz	Fastqsanger.gz
	ERR5000374.fastq.gz	Fastqsanger.gz

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RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

Project description:RNA-sequencing was performed to determine the differences between cells that contain mutant p53 and a transactivation deficient mutant of p53 to determine why the TAD mutant cells don't form tumors.

2020-12-18 | E-MTAB-9833 | biostudies-arrayexpress

RNAseq analysis for transcriptomes of ATO treated U937 cell lines expressing 10 type 1 p53 mutants, type-3 p53-R273H, p53 null, or p53 wild-type

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Project description:A total of 58 genes were up-regulated (> 1.5 fold-change) while 117 genes were down-regulated Microarray experiments were performed in duplicate as follows: MDA-MB-468 cells were transduced with lentiviral shRNA targeting endogenous p53-R273H mutant (p53si-1)or a non-targeting shRNA (NS). Total RNA from cells was extracted using Qiagen RNA isolation kit (Qiagen, Valencia, CA, USA) according to the manufacturersâ protocol. RNA purity was examined by spectrophotometric determination at 260/280 nm. The microarray hybridizations were carried out using the Affymetrix Human Gene 1.0 ST arrays.

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Project description:Mutations effects on p53 isoforms’ activities remain largely unknown, although they are mutated in 92% of TP53 mutant cancers. Therefore, exploring the effect of mutations on p53 isoforms activities is a critical, albeit unexplored area in the p53 field. Current glioblastoma treatments, including temozolomide chemotherapy and radiations, induce cellular senescence through a p53-dependent mechanism. Nevertheless, GBMs still have a poor 6.8% five-year survival indicating a need to better understand underlying mechanisms affecting the response to treatments. The progression from low-grade astrocytoma to glioblastoma is accompanied by TP53 mutations. Since Δ133p53α prevents cellular senescence, studying the impact of its mutation in glioblastoma is relevant to determine if it affects the progression and response to treatment of GBM cells. In this aim, we stably overexpressed wild-type (WT) Δ133p53α in WT glioblastoma multiforme (GBM) cells, and Δ133p53α R273H in R273H mutant GBM cells. We used mRNA-sequencing to identify mutant Δ133p53α-specific target genes. We examined proliferation, invasion, DNA repair, apoptosis, and senescence regulation by WT and mutant Δ133p53α. All results were confirmed by siRNA knock-down. Finally, using TCGA data, we investigated the association of the mutant Δ133p53α-specific target genes to clinical outcome of GBM and low-grade glioma (LGG) patients. This study provides the first and most in-depth characterization of a mutant p53 isoform’s activities to date and demonstrate that mutant Δ133p53α R273H is an active contributor to glioblastoma carcinogenesis and response to treatment. Furthermore, by discovering the link between TP53 mutation and IL4I1/IDO1/AhR pathway, we show strong evidence of Δ133p53α R273H clinical relevance in mutant TP53 glioblastoma development and aggressiveness, and as a potential therapeutic target and biomarker.

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| PRJNA756908 | ENA

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