Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157951 | GEO | 2021/02/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

p53 influences 5-FU-induced chromatin accessibility [ChIP-seq]

Project description:5-Fluorouracil (5-FU) is one of the most common drugs used in chemotherapy because of its efficacy and stability. However, 5-FU has been known to work on only 10~15% of colon cancer patients. Therefore, the study of 5-FU sensitivity study is necessary to increase the survival of colon cancer patients. p53 is one of the factors that effect on drug sensitivity. Main function of p53 has been focused on transcription activity in cell death. Numerous drug related studies show that expression of wild-type p53 increases drug sensitivity in various cancer types through inducing apoptotic signaling pathways. Currently, it has been reported that p53 has both transcriptional and non-transcriptional activities in apoptosis. However, most studies about p53 non-transcriptional activities in apoptosis are mainly focused on p53 induced mitochondrial outer membrane permeabilization, triggering the release of pro-apoptotic factors. The chromatin structure and organization have strongly attracted because of their impacts in cellular phenotypes. Recent studies have been shown that changes in chromatin accessibility affect cell phenotypes for external stimuli. Since p53 plays an important role in drug sensitivity and 5-FU is an external stimulus for cancer cells, we hypothesized that p53 may effect on 5-FU sensitivity through different regulation of chromatin accessible regions between TP53-WT and TP53-KO cells. To determine the effect of p53 on chromatin accessibility modification associated with 5-FU sensitivity, ATAC-seq and RNA-seq were performed under 5-FU treatment on TP53-WT as drug sensitive and TP53-KO as drug resistant HCT116 cells. In this study, we found that 5-FU induces chromatin accessibility in both TP53-WT and TP53-KO cells. Moreover, our results show that 5-FU induced chromatin accessibility increases expression of apoptotic genes in TP53-WT HCT116 cells through p53 non-transcriptional activity in nucleus.

2021-02-10 | GSE157950 | GEO

p53 influences 5-FU-induced chromatin accessibility [ATAC-seq]

2021-02-10 | GSE157949 | GEO

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

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

| PRJNA663474 | ENA

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

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

5-Fluorouridine restores functional full-length p53 in TP53 nonsense mutant human tumor cells (RNA-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 | GSE196710 | GEO

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

2022-12-01 | GSE196709 | GEO

TP53 promotes lineage commitment of human embryonic stem cells through ciliogenesis and sonic hedgehog signaling [RNA-Seq]

Project description:H9 WT ESCs or TP53 KO (Clone 1) ESCs were injected subcutaneously into mice for teratoma formation. 6-8 weeks later, teratomas were isolated and total RNA was purified. TruSeq library preparation kit from Illumina was used to make libraries for RNA-Seq. NGS sequencing on Illumina NextSeq 500 was performed and data was analyzed to determine changes in transcriptome between WT and TP53 KO teratoma cells.

2022-02-16 | GSE168678 | GEO

Transcription profiling of human HCT116 parental cells treated with 5-FU or SN38 and non-treated parental cells, 5-FU resistant and SN39 resistant cells

Project description:The transcriptional profiles of the HCT116 parental cells following treatment with either 5-FU or SN38 for 24h were assessed. In addition, basal comparisons between HCT116 parental and HCT116 5-FU -resistant and HCT116 SN38-resistant cells were also assessed.

2009-03-30 | E-MEXP-1691 | biostudies-arrayexpress

Effects on gene expression of RNA polymerase I inhibitor CX-5461 in control and TP53-knockout cell lines of multiple myeloma

Project description:Multiple myeloma cell lines MM1S and MOLP8 were modified by zinc finger nucleases targeting exon 7 of the TP53 DNA binding domain. Knockout (KO) clones were isolated by limiting dilution, identified by TP53 resequencing, and confirmed by Western blotting. KO and unmodified (WT) clones were then either treated with vehicle or 200 nM CX-5461 for 48 hours for gene expression profiling (GEP).

2019-10-01 | GSE73665 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data