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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

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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]

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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.

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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

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

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p53-regulated networks of protein, mRNA, miRNA and lncRNA expression revealed by integrated pSILAC and NGS analyses

Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3â??-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.

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