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Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [mRNA]

ABSTRACT: Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [mRNA]

PROVIDER: PRJNA575234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10210727_1.fastq.gz	Fastqsanger.gz
	SRR10210727_2.fastq.gz	Fastqsanger.gz
	SRR10210728_1.fastq.gz	Fastqsanger.gz
	SRR10210728_2.fastq.gz	Fastqsanger.gz
	SRR10210729_1.fastq.gz	Fastqsanger.gz

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Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells

Project description:Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells

| PRJNA575229 | ENA

Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [miRNA-Seq]

Project description:Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [miRNA-Seq]

| PRJNA575232 | ENA

Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [mRNA]

Project description:Unlike other EBV-associated human tumors, nearly 100% wild-type p53 gene is found in NPC, p53 protein is also frequently found to accumulate in NPC biopsies. However, the role of p53 in EBV-positive nasopharyngeal carcinoma is unclear. The expression profiles of mRNAs and miRNAs of EBV-positive NPC cells are unknown. To elucidate the function of p53 in EBV-positive NPC, we used the CRISPR-Cas9 gene editing system to p53 knockout C666-1 cells with Epstein-Barr virus and performed mRNA and miRNA sequencing in p53 KO C666-1 and their control cells. Gene Ontology (GO), KEGG and STRING analyses were implemented to identify significant functions, pathways of differentially expressed mRNAs. Through comparative analysis of p53-regulated genes from EBV-positive C666-1 cells and EBV-negative HONE2 cells with p53 target genes from 16 high throughput data sets, we found that the number of target genes and KEGG pathways downregulated by p53 in EBV-positive C666-1 cells were much less than in EBV-negative HONE2 cells, but “p53 signaling pathway” and related cell cycle arrest and apoptosis genes were significantly downregulated after knockout of p53 gene in C666-1 cells. To explore the effect of p53 on cell cycle and apoptosis, we established stable p53 C666-1-KO cell lines with stable expression of exogenous p53-WT and their control cell lines. Using the established cell lines, we observed that stable expression of p53 repressed cell proliferation, increased cell apoptosis and blocked G1/S phase progression. In conclusion, our results show that the accumulated p53 protein in EBV-positive C666-1 cells still has some tumour suppressor functions such as blocking cell-cycle progression and promoting apoptosis, but the ability of p53 to downregulate gene expression is inhibited.

2021-03-01 | GSE138258 | GEO

Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells [miRNA-Seq]

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Bioinformatic Analysis of mRNA and miRNA Expression Patterns In p53 Knock-out C666-1 cells

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

2021-03-01 | GSE138259 | GEO

Acute p53 knock-out in mouse liver

Project description:Here we investigated the effects of acute p53 deletion on the fasting response in mice.

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Differential expression of mRNA in Tax1BP1 knock-out mice [mRNA]

Project description:To further characterize differential expression of miRNA and mRNA levels in livers of 12 weeks old male Tax1BP1 wildtype and knock-out mice, the untreated mice were sacrificed and miRNA and mRNA levels were determined

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Transcription profiling of p53 knock-out mouse to analyse neural stem cell (neurosphere) prolifieration

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Differential expression of miRNA and mRNA in Tax1BP1 knock-out mice

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Transcription profiling of mouse Atm-/-,mTerc-/-,p53-/- triple knock-out lymphoma vs normal

Project description:Highly rearranged and mutated cancer genomes present major challenges in the identification of pathogenetic events driving the cancer process. Here, we engineered lymphoma-prone mice with chromosomal instability to assess the utility of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations. Integrating with targeted re-sequencing, our comparative oncogenomic studies efficiently identified FBXW7 and PTEN as commonly deleted or mutated tumor suppressors in human T-cell acute lymphoblastic leukemia/lymphoma (T-ALL). More generally, the murine cancers acquire widespread recurrent clonal amplifications and deletions targeting loci syntenic to alterations present in not only human T-ALL but also diverse tumors of hematopoietic, mesenchymal and epithelial types. These results thus support the view that murine and human tumors experience common biological processes driven by orthologous genetic events as they evolve towards a malignant phenotype. The highly concordant nature of genomic events encourages the use of genome unstable murine cancer models in the discovery of biologically relevant driver events in human cancer. Experiment Overall Design: 18 lymphoma samples from Atm-/-, mTerc-/-, p53-/- triple knock-out mice were analyzed. 3 week old hymus RNA from healthy mice of p53 Hets was used as reference. Each sample was hybridized with dye-swap replica.

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