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

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

PROVIDER: PRJNA663474 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12642015_1.fastq.gz	Fastqsanger.gz
	SRR12642015_2.fastq.gz	Fastqsanger.gz
	SRR12642016_1.fastq.gz	Fastqsanger.gz
	SRR12642016_2.fastq.gz	Fastqsanger.gz
	SRR12642017_1.fastq.gz	Fastqsanger.gz

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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

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type HCT116 and MTF1-KO HCT116 injected tumor Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to use RNA-seq to find differences between WT and MTF1-KO tumor in colorectal cancer Methods: HCT116 cells and MTF1-KO HCT116 cells were injected subcutaneously into the back of NSG mice at 2x106 cells/recipient , At day 24 after injection，Tumor tissue were isolated from infected recipients，and Total RNA was collected. Besides,about 5x106 cultured HCT116 cells and MTF1-KO HCT116 cells were collected for total RNA isolation ,and sent all of them for sequencing. Conclusions: Our study represents the transcriptome difference between WT HCT116 tumor and MTF1-KO HCT116 tumor has a very positive significance for the pathological process of colorectal cancer，especially for cell adhension

2022-12-15 | GSE190435 | 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

Effect of wtp53-reactivating drug RITA on HCT116 cells

Project description:Since its discovery as a tumour suppressor some fifteen years ago, the transcription factor p53 has attracted paramount attention for its role as “the guardian of the genome”. TP53 mutations occur so frequently in cancer, regardless of patient age or tumour type, that they appear to be part of the life history of at least 50% of human tumours. In most tumours that retain wild-type p53, its function is inactivated due to deregulated HDM2, a protein which binds to p53 and which can inhibit the transcriptional activity of p53 and induce its degradation. RITA is a low-molecular-weight compound which addresses the second group of tumours retaining functionally reactive wt p53. It was found in a screening of the National Cancer Institute (NCI) library of low-molecular-weight compounds based on its ability to selectively kill wtp53-containing cells. RITA binds directly to p53 and diplaces its main destructor Mdm2, as well as inducing a shift in the conformation of p53. This is in contrast to the wtp53-reactivating compound Nutlin3a, which targets Mdm2, inhibiting its ability to degrade p53. Using microarray technology we have explored the effect of RITA on the transcriptome of isogenic cell-lines with knocked-out (KO) or intact (WT) TP53. While the effects on KO cells are below detection limit, the effects on WT cells are profound. The known p53 targets induced are predominately apoptotic, in contrast to the genes affected by Nutlin3a, which are exclusively growth-arrest genes. Keywords: Antitumor agent HCT116 parental and HCT116 p53-null (HCT116 TP53-/-) cells were subjected to treatment with 1uM RITA for 12h, or left untreated. The experiment was done in three independent biological replicates.

2009-02-28 | E-GEOD-11578 | biostudies-arrayexpress

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Project description:mRNA was sequenced from HCT116 MYC 3' TBE1 (WT) and KO cells to identify genes differentially expressed after deletion of the MYC 3' TBE1

2016-05-24 | GSE70833 | GEO

Epigenome analysis of human gastroesophageal junction (GEJ) organoids TP53/CDKN2A KO

Project description:Inactivation of the tumor suppressor genes TP53 and CDKN2A occurs early during GEJ tumorigenesis. However, due to a paucity of GEJ-specific disease models, cancer-promoting consequences of TP53 and CDKN2A inactivation at the GEJ have been incompletely characterized. Here we report the development of the first wild-type primary human GEJ organoid model, as well as a CRISPR-edited transformed GEJ organoid model. CRISPR/Cas9 engineering to inactivate TP53 and CDKN2A (TP53/CDKN2A KO) in GEJ organoids induced morphologic dysplasia as well as pro-neoplastic features in vitro and tumor formation in vivo. Notably, lipidomic profiling identified several Platelet-Activating Factors (PTAFs) among the most upregulated lipids in CRISPR-edited organoids; and importantly, PT AF/PT AFR abrogation by siRNA knockdown or a pharmacologic inhibitor (WEB2086) significantly blocked proliferation and other pro-neoplastic features of TP53/CDKN2A KO GEJ organoids in vitro and tumor formation in vivo. In addition, murine xenografts derived from Eso26, an established esophageal adenocarcinoma (EAC) cell line, were suppressed by WEB2086. Mechanistically, TP53/CDKN2A dual inactivation disrupted both the transcriptome and the DNA methylome, likely mediated by key transcription factors, particularly Forkhead Box M1 (FOXM1). Importantly, FOXM1 activated PTAFR transcription by binding to the PTAFR promoter, further amplifying the PTAF-PTAFR pathway. In summary, we established a robust model system for investigating early GEJ neoplastic events, identified crucial metabolic and epigenomic changes occurring during GEJ model tumorigenesis, and discovered a potential cancer-therapeutic strategy, while providing insights into pro-neoplastic mechanisms associated with TP53/CDKN2A inactivation in early GEJ neoplasia.

2022-11-02 | GSE216814 | GEO

Expression profiles of HCT116 colorectal cancer cells and HCT116-derived CDKN1A (p21) knockout (ko) cells.

Project description:Gene expression profiles were obtained via Nanostring nCounter Expression Assay (PanCancer Progression Panel, Nanostring Technologies, Hamburg, Germany). We aimed to obtain a gene expression signature associated to the kockout of p21 (i.e. Cyclin Dependent Kinase Inhibitor 1A, CDKN1A) in colorectal carcinoma samples and its association with of epithelial-mesenchymal transition (EMT). We analysed and compared three independent cultures of HCT116 p21 wt cells and three HCT116 p21-/- ko cells.

2019-11-01 | GSE135923 | GEO

RNA-seq for HCT116 and KO-CREB1 cells

Project description:RNA-seq for HCT116 and KO-CREB1 cells

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RNA-sequencing data of HCT116-wild type (WT), HCT116-A20 knockout (KO) and HCT116-A20-KO-rescue (OE) cells

Project description:Purpose: The goals of this study are to compare the transcriptome profiling (RNA-seq) of different A20 expression in HCT116 cells, to find potiential target genes for A20 mediated immnue escape. Results: There were 352 genes altered after A20 was knocked out with the log-fold >2 or <-2 compared to WT cells, and p value<0.01 . And 143 genes changed after rescued the expression of A20 in A20-KO cells compared to A20-KO cells. Among these altered genes, 13 genes were changes consistently. Conclusion:Gain- and loss-A20 functional studies proved that A20 could decrease the ¡°eat-me¡± signal calreticulin (CRT) protein on cell membranes via stabilizing stanniocalcin 1 (STC1). Mechanistically, A20 inhibited the degradation of STC1 protein which could capture the CRT inside cell rather than to translocated to cell membrane.

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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

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