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Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

ABSTRACT: Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

PROVIDER: PRJNA701951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13712415.fastq.gz	Fastqsanger.gz
	SRR13712416.fastq.gz	Fastqsanger.gz
	SRR13712417.fastq.gz	Fastqsanger.gz
	SRR13712418.fastq.gz	Fastqsanger.gz
	SRR13712419.fastq.gz	Fastqsanger.gz

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Similar Datasets

Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

Project description:Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

| PRJNA701951 | ENA

Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

Project description:The transcription factor p53 exerts its tumor suppressive effects through transcriptional activation of numerous target genes controlling cell cycle arrest, apoptosis, cellular senescence and DNA repair. In addition, there is evidence that p53 influences the translation of specific mRNAs, including translational attenuation of ribosomal protein synthesis and translational activation of MDM2. A challenge in the analysis of translational control is that changes in mRNA abundance exert a kinetic (passive) effect on ribosome densities. In order to separate these passive effects from active regulation of translation efficiency in response to p53 activation, we conducted a comprehensive analysis of translational regulation by comparative analysis of mRNA levels and ribosome densities upon DNA damage induced by neocarzinostatin in wild-type and TP53-/- HCT116 colorectal carcinoma cells. Thereby, we identified a specific group of mRNAs whose translation is actively up-regulated in response to p53 activation, the majority of which are transcribed from p53 target genes including MDM2, SESN1 and CDKN1A. By subsequent polysome profile analysis, we could demonstrate that a p53-dependent switch in transcript isoform expression is responsible for translational activation of SESN1, whereas translational activation of CDKN1A occurs through a trans-acting mechanism that affects multiple transcript isoforms.

2022-04-13 | GSE166783 | GEO

nascent proteome analysis of HCT116 TP53 wild type and TP53 knockout cells treated with Neocarcinostatin (NCS) for 6h

Project description:In order to investigate the potential role of TP53 in regulating translation, HCT116 wild type and TP53 knockout cells were analyzed using both RNA sequencing, Ribosome sequencing and nascent proteome analysis. The cells were treated with 0.2 µg/ml Neocarcinostatin (NCS) to induce DNA damage and activate TP53.

2022-04-27 | PXD029512 | Pride

RNAseq of mutant TP53 HCT116 cell line clones generated via CRISPR editing

Project description:To compare the impact of several TP53 mutant variants in an isogenic setting, different TP53 mutations were introduced in HCT116 colorectal carcinoma cells. This parental cell line is wild-type for TP53 and shows a prototypical p53 response. To ensure unambigous genotype-phenotype correlations, the cell were haploidized prior to CRISPR-editing by introducing inactivating deletions of intronic splicing into one of the two TP53 alleles, leaving only one functional copy of TP53. The remaining TP53 allele was altered by inserting a LoxP-flanked transcriptional stop cassette (Lox-Stop-Lox, LSL) into intron 4, which allowed reversible silencing of TP53 expression. The LSL cassette was then specifically targeted with CRISPR/Cas9 to introduce a variety of different mutant p53 alleles. The competency of the mutated p53 allele to induce a p53 response upon activation using Nutlin-3a was then assessed in an RNAseq experiment.

2024-10-16 | E-MTAB-12734 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of TP53-WT and TP53-KO HCT116 cells transcriptomes [RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare TP53-WT and TP53-KO HCT116 cells transcriptome profiling (RNA-seq) under 5-FU treatment condition and to evaluate the correlation between transcriptome profileing and chromatin accessibility under 5-FU treatment. Methods: HCT116 cell profiles of TP53-WT and TP53- KO were generated by deep sequencing, in duplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform levels: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA). Conclusions: Our study represents the detailed analysis of TP53-WT and TP53-KO HCT116 cell transcriptomes under 5-FU treatment with different timepoint, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that RNA-seq offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a TP53-WT and TP53-KO cells with and without 5-FU treatment in different timepoint. We conclude that NGS based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2021-02-10 | GSE157951 | GEO

Ribo-seq of human colorectal cancer cell line HCT116/L-OHP against HCT116

Project description:Ribo-seq of human colorectal cancer cell line HCT116/L-OHP against HCT116

| PRJEB46746 | ENA

Amplicon-Screening of genomic DNA regions of mutants in the Exon5 R175 position of TP53 in HCT116 cells generated via CRISPR editing

Project description:To compare the impact of CRISPR-egineered R175 TP53 mutant variants in HCT116 and H460 cells, mutations at the amino acid position 175 were generated systematically by CRISP/Cas9 editing. Here, genomic amplicon regions covering the TP53 Exons 5 were sequenced via targeted sequencing.

2024-10-16 | E-MTAB-14322 | biostudies-arrayexpress

Amplicon-Screening of exonic RNA in exon-wide mutant cell libraries of mutant TP53 (Exons 5, 6, 7, 8) in HCT116 cells generated via CRISPR editing

Project description:To compare the impact of TP53 mutant variants in exon-wide mutant cell libraries, comprehensive mutome libraries of TP53 affecting the Exons 5, 6, 7 and 8 were generated systematically by CRISP/Cas9 editing in HCT116 colorectal carcinoma cells.

2024-10-16 | E-MTAB-12861 | biostudies-arrayexpress

Amplicon-Screening of exonic DNA regions in exon-wide mutant cell libraries of mutant TP53 (Exons 5, 6, 7, 8) in HCT116 cells generated via CRISPR editing

2024-10-16 | E-MTAB-12857 | biostudies-arrayexpress

5-Fluorouridine restores functional full-length p53 in TP53 nonsense mutant human tumor cells (Ribo-Seq)

Project description:The tumor suppressor gene TP53 is mutated in approximately half of all human tumors. Of those, around 10% are nonsense mutations that produce truncated and inactive p53 protein. Induction of translational readthrough is a promising approach for rescuing full-length p53 and thereby eliminate tumor cells with nonsense mutant TP53. To find novel nonsense mutant TP53 readthrough-inducing compounds with a tolerable toxicity profile, we performed an in silico screening of data at the National Cancer Institute database and identified 5-Fluorouracil (5-FU). We show here that 5-FU induces full-length p53 in human tumor cells carrying R213X nonsense mutant TP53 and that this activity is mediated by its metabolite 5-Fluorouridine (FUr). Ribo-seq analysis validated induction of translational readthrough by FUr. We also show that FUr is incorporated into RNA where it potentially allows base pairing of Arg tRNA at the R213X UGA premature termination codon. Full-length p53 rescued by FUr is transcriptionally active and triggers p53-dependent cell death. Moreover, treatment with 5-FU or FUr restores full-length p53 expression in TP53 R213X mutant human tumor xenografts in vivo. Our results suggest that induction of readthrough by 5-FU/FUr could contribute to therapeutic efficacy in patients with TP53 nonsense mutant tumors.

2022-12-01 | GSE196709 | GEO

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