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Temporal gene regulation by p53 is associated with the rotational setting of its binding motifs in nucleosomes

ABSTRACT: HCT116 cells treated with 5-FU along with DMSO and non-treatment controls using time-course RNA-seq were used to investigate target genes regulated by p53 at the different timepoints.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157300 | GEO | 2021/03/30

REPOSITORIES: GEO

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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]

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Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246

Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control

2018-02-09 | MSV000082047 | MassIVE

Temporal gene regulation by p53 is associated with the rotational setting of its binding motifs in nucleosomes

Project description:Temporal gene regulation by p53 is associated with the rotational setting of its binding motifs in nucleosomes

| PRJNA660785 | ENA

Global analysis of p53-regulated transcription reveals its direct targets and unexpected regulatory mechanisms (GRO-Seq)

Project description:GRO-seq of HCT116 cells treated with Nutlin to activate p53 HCT116 cells were treated with Nutlin or DMSO for 1 hour

2014-05-15 | E-GEOD-53964 | biostudies-arrayexpress

Inactivation of Oncogenic cAMP-specific Phosphodiesterase 4D by miR-139-5p in Response to p53 Activation

Project description:Investigation of microRNA expression level changes in human colon cancer cell lines in response to p53 activation by Inauhzin (INZ), and identification of novel p53 target microRNAs. HCT116 p53+/+ and HCT116 p53-/- cells were treated with DMSO or 4Î¼M INZ and harvested at 18 hours post treatment. Cells were then homogenized in TriZol reagents. Duplicates were included for each sample. Total RNA was extracted by following the manufacturerâs standard instructions (Invitrogen).

2016-07-20 | E-GEOD-79099 | biostudies-arrayexpress

Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

Project description:Microarray-based gene expression analysis of HCT116 p53+/+ and HCT116 p53−/− treated with doxorubicin to activate p53 in time-dependent manner.

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RNA-seq of depletion Mina53 in HCT116 p53+/+ cells and HCT116 p53-/- cells

Project description:We report the signaling pathway of Mina53 by depleting Mina53 in HCT116 p53+/+ cells and HCT116 p53-/- cells based on RNA-sequencing.

2024-12-01 | GSE214730 | GEO

Temporal gene regulation by p53 is associated with the rotational setting of its binding sites in nucleosomes.

Project description:The tumor suppressor protein p53 is a DNA-binding transcription factor (TF) that, once activated, coordinates the expression of thousands of target genes. Increased p53 binding to gene promoters occurs shortly after p53 activation. Intriguingly, gene transcription exhibits differential kinetics with some genes being induced early (early genes) and others being induced late (late genes). To understand pre-binding factors contributing to the temporal gene regulation by p53, we performed time-course RNA sequencing experiments in human colon cancer cell line HCT116 treated with fluorouracil to identify early and late genes. Published p53 ChIP fragments co-localized with the early or late genes were used to uncover p53 binding sites (BS). We demonstrate that the BS associated with early genes are clustered around gene starts with decreased nucleosome occupancy. DNA analysis shows that these BS are likely exposed on nucleosomal surface if wrapped into nucleosomes, thereby facilitating stable interactions with and fast induction by p53. By contrast, p53 BS associated with late genes are distributed uniformly across the genes with increased nucleosome occupancy. Predicted rotational settings of these BS show limited accessibility. We therefore propose a hypothetical model in which the BS are fully, partially or not accessible to p53 in the nucleosomal context. The partial accessibility of the BS allows subunits of a p53 tetramer to bind, but the resulting p53-DNA complex may not be stable enough to recruit cofactors, which leads to delayed induction. Our work highlights the importance of DNA conformations of p53 BS in gene expression dynamics.

| S-EPMC8098069 | biostudies-literature

Expression profile of HCT116 p53+/+ and P53-/- cells treated with Leptomycin B

Project description:HCT116 wild type cells express p53. The isogenic HCT116 p53KO cells have the p53 gene knocked out. Cells were treated for 16 hours. Dosages for leptomycin B treatment was 2 nM and 20 nM.

2010-07-31 | GSE17472 | GEO

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