P53 influences 5-FU-induced chromatin accessibility [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA663473 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12642058_1.fastq.gz | Fastqsanger.gz | |||
| SRR12642058_2.fastq.gz | Fastqsanger.gz | |||
| SRR12642059_1.fastq.gz | Fastqsanger.gz | |||
| SRR12642059_2.fastq.gz | Fastqsanger.gz |
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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
Project description:p53 influences 5-FU-induced chromatin accessibility [ATAC-seq]
| PRJNA663471 | ENA
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.
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Project description:We accessed the cell type specificity of p53 by directly measuring DNA binding in twelve cell lines in response to ionizing radiation. We find that that vast majority of binding sites are occupied across all cells lines uniformly, in contrast to p53 regulated gene expression which shows great diversity in the same context. We further identify a subset of p53 binding sites that are more restricted, appearing in one or a few cell lines. We find that chromatin accessibility explains much of these differential binding events.
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Project description:We used ATAC-seq to detect changes in chromatin accessibility and nucleosome positioning around the MYC gene during the DNA double-strand break response in human cells and the dependence of these changes on p53. We found that, in the region ~50 kb downstream of MYC where p53 binds strongly, chromatin accessibility as measured by ATAC-seq fragment density increased during the DNA DSB response, corresponding to the removal of a single nucleosome. These results are consistent with increased accessibility of a distal regulatory element at this locus that is dependent on DNA damage and p53 expression. At the MYC promoter region there is a p53-dependent decrease in chromatin accessibility in response to DSBs, even in the absence of a direct p53 binding site near the region. While both the P1 and P2 promoters of MYC are relatively free of nucleosomes in MCF-7 sh-p53 cells, both promoters are occluded in cells expressing WT levels of p53, with an increase of nucleosomal occlusion in response to DNA damage. This supports the hypothesis that MYC repression during the DNA DSB response results from nucleosomal occlusion of both the P1 and P2 promoters.
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Project description:To investigate how mutant p53 regulates gene transcription in HSPCs, we performed ATAC-seq assays in LSKs to identify differential regions of chromatin accessibility. We obsreved approximately 600 peaks significantly increased chromatin accessibility in mutant p53 LSKs compared to wild type p53 LSKs.
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Project description:Spermatogonial stem cells (SSCs) could transform into pluripotent state in long term culture without introduction of exogenous factors. And p53 deficiency rescued SSCs from extensive cell apoptosis during transformation induced by rewriting of methylation profiles in SSCs. Notably, p53 is believed as a key bottle-neck for reprogramming. Based on these studies, we compared the difference of chromatin accessibility between SSCs from wild type and p53 deficient SSCs mice using ATAC-seq, to explore the potential mechanism at chromosome level. And RNA-Seq was subsequently exerted to verify the predicted genes and related pathways in SSCs transformation. This result further reveals the role of p53 in regulating SSCs fates, which provide hints new insight for understanding the biological characteristics of germline stem cells, basic and clinic researchand molecular mechanisms of reprogramming and tumorigenesis.
2021-10-08 | E-MTAB-10012 | biostudies-arrayexpress
Project description:Spermatogonial stem cells (SSCs) could transform into pluripotent state in long term culture without introduction of exogenous factors. And p53 deficiency rescued SSCs from extensive cell apoptosis during transformation induced by rewriting of methylation profiles in SSCs. Notably, p53 is believed as a key bottle-neck for reprogramming. Based on these studies, we compared the difference of chromatin accessibility between SSCs from wild type and p53 deficient SSCs mice using ATAC-seq, to explore the potential mechanism at chromosome level. And RNA-Seq was subsequently exerted to verify the predicted genes and related pathways in SSCs transformation. This result further reveals the role of p53 in regulating SSCs fates, which provide hints new insight for understanding the biological characteristics of germline stem cells, basic and clinic researchand molecular mechanisms of reprogramming and tumorigenesis.
2021-10-08 | E-MTAB-10013 | biostudies-arrayexpress
Project description:Chromatin organization is a highly orchestrated process that influences gene expression, in part by modulating access of regulatory factors to DNA and nucleosomes. We found that the chromatin accessibility regulator HMGN1, a target of recurrent DNA copy gains in leukemia, controls myeloid differentiation. HMGN1 amplification was associated with increased accessibility, expression, and histone H3K27 acetylation of loci important for hematopoietic stem cell (HSC) function and AML, such as HoxA cluster genes. In vivo, HMGN1 overexpression was linked to decreased quiescence and increased HSC activity in bone marrow transplantation. HMGN1 overexpression also cooperated with the AML-ETO9a fusion oncoprotein to impair myeloid differentiation and enhance leukemia stem cell (LSC) activity. Inhibition of histone acetyltransferases CBP/p300 relieved the HMGN1-associated differentiation block. These data nominate factors that modulate chromatin accessibility as regulators of HSCs and LSCs and suggest that targeting HMGN1 or its downstream effects on histone acetylation could be therapeutically active in AML.
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