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Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

ABSTRACT: We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58714 | GEO | 2014/11/21

SECONDARY ACCESSION(S): PRJNA253215

REPOSITORIES: GEO

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Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.

2014-11-21 | E-GEOD-58714 | biostudies-arrayexpress

Distinct p53 Genomic Binding Patterns in Normal and Cancer-derived Human Cells

Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells. Identification of genomic p53 binding sites in normal human cells by ChIP-seq.

2011-12-08 | E-GEOD-31558 | biostudies-arrayexpress

Distinct p53 Genomic Binding Patterns in Normal and Cancer-derived Human Cells

2011-12-08 | GSE31558 | GEO

Epigenetically Silenced Genes Found Using Methylated DNA Immunoprecipitation in Colon Cancer Cells Deficient in DNMTs

Project description:CpG island promoter hypermethylation of tumor suppressor genes is a common hallmark of human cancer, and new large-scale epigenomic technologies might be useful in our attempts to define the complete DNA hypermethylome of tumor cells. Here we report a functional search for hypermethylated CpG islands using the colorectal cancer cell line HCT-116, in which two major DNA methyltransferases, DNMT1 and DNMT3b, have been genetically disrupted (DKOcells). Using methylated DNA immunoprecipitation (MeDIP) methodology in conjunction with promoter microarray analyses we found that DKO cells experience a significant loss of hypermethylated CpG islands. Further characterization of these candidate sequences demonstrates CpG island promoter hypermethylation and silencing of genes with potentially important roles in tumorigenesis, such as the Ras guanine-nucleotide release factor RASGRF2, the apoptosis-associated basic helixloop transcription factor BHLHB9, and the homeobox gene HOXD1. Hypermethylation of these genes occurs already in premalignant lesions and accumulates during tumorigenesis. Thus, our results demonstrate the usefulness of DNMT genetic disruption strategies combined with MeDIP in searching for unknown hypermethylated candidate genes in human cancer that might aid our understanding of the biology of the disease and be of potential translational use. Keywords: Human Proximal Promoter Array; DNA Methylation Comparative experiment: methylated DNA immunoprecipitated/INPUT(Total Genomic DNA) from the colon cancer cell line HCT116 wild type vs methylated DNA imonoprecipitated/INPUT from the colon cancer cell line HCT116 DNMT1/3b doubleknockout (DKO)

2010-05-27 | E-GEOD-9267 | biostudies-arrayexpress

Homo sapiens

Project description:Chromatin dynamics of p53 binding sites in IMR90

| PRJNA253315 | ENA

Genomewide analysis of the human p53 transcriptional network unveils a lncRNA tumor suppressor signature (RNA-seq)

Project description:We report the application of high-throughput sequencing to performed the p53 regulated trancriptome in HCT116 colon cancer cells treated with the DNA damage 5FU. To study the direct targets of p53 we performed ChIP-seq to deterrmined the p53 biding sites and associated with the expression levels. With this study we identified the new genomic regions regulated by p53 and with special attention in those regions that are non coding and are differentially expressed by the DNA damage drug. Description of the p53 transcriptome in HCT116 colon cancer cell line. The RNA-seq libraries were prepared from purified poly-A+ RNA from untreated and 5-Fluorouracil treated p53 +/+ HCT116 cells for 4 and 12h, including two independent samples for the time 12h. Paired-end and strand specific RNA sequencing libraries were prepared according to Illumina instructions and sequenced on HiSeq 2000 (Ilumina) with sequence length of 150 bp. Raw sequencing data were alignment to the human genome (hg19) using Tophat mapper.

2014-12-22 | E-GEOD-58507 | biostudies-arrayexpress

Crotonylomics sequencing of human colon cancer cell lines

Project description:P53 mutation is closely associated with the occurrence and progression of colon cancer. In this project, we did crotonylomics sequencing by using human colon cancer homologous cell line pair-HCT116+/+(with wild type p53) and HCT116-/- (with null p53). Crotonylomics sequencing results showed that p53 deficiency regulated crotonylation of non-histone proteins.

2024-05-22 | PXD047258 | Pride

"Calling Cards" for DNA-binding proteins in mammalian cells

Project description:The ability to chronicle transcription factor binding events throughout the development of an organism would facilitate mapping of transcriptional networks that control cell fate decisions. We describe a method for permanently recording protein-DNA interactions in mammalian cells. We endow transcription factors with the ability to deposit a transposon into the genome near to where they bind. The transposon becomes a M-bM-^@M-^\Calling CardM-bM-^@M-^] the transcription factor leaves behind to record its visit to the genome. The locations of the Calling Cards can be determined by massively-parallel DNA sequencing. We show that the transcription factor SP1 fused to the piggyBac transposase directs insertion of the piggyBac transposon near SP1 binding sites. The locations of transposon insertions are highly reproducible, and agree with sites of SP1-binding determined by ChIP-seq. Genes bound by SP1 are more likely to be expressed in the HCT116 cell line we used, and SP1-bound CpG islands show a strong preference to be unmethylated. This method has the potential to trace transcription factor binding throughout cellular and organismal development in a way that has heretofore not been possible. These data contain mapped insertion sites from the piggyBac (PB) transposon into HCT116 cell line and sequenced using an Illumina GAII analyzer. The first set contains the insertion sites of transposons mapped from the wild-type PB transposase and the second set contains the insertion sites of transposons mapped with the PB transposase fused to the transcription factor SP1. Other sequencing data present are ChIP-seq data for SP1 in the HCT116 cell line and RNA-seq data.

2011-12-31 | E-GEOD-34791 | biostudies-arrayexpress

p53 ChIP-seq in Nutlin-treated HCT116, MCF7, and SJSA cell lines

Project description:To identify genomic loci occupied by p53, we performed p53 ChIP-seq analysis of colorectal carcinoma cell line HCT116, breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin.

2017-08-22 | GSE86164 | GEO

Clustering of CpG islands constitutes an important determinant of the interphase chromosome 3D organization [ChIP-Seq]

Project description:Using 4C-Seq experimental procedure we have characterized, in cultured chicken lymphoid and erythroid cells, genome-wide patterns of spatial contacts of several CpG islands scattered along the chromosome 14. A clear tendency for interaction of CpG islands present within the same and different chromosomes has been observed. Accordingly, preferential spatial contacts between Sp1 binding motifs, and other GC-rich genomic elements including DNA sequence motifs capable to form G-quadruplexes were demonstrated. On the other hand, an anchor placed in gene/CpG islands-poor area was found to form spatial contacts with other gene/CpG islands-poor areas within chromosome 14 and other chromosomes. These results corroborate the two compartments model of interphase chromosome spatial organization and suggest that clustering of CpG islands harboring promoters and origins of DNA replication constitutes an important determinant of the 3D organization of eukaryotic genome in the cell nucleus. Using ChIP-Seq experimental procedure we have mapped genome-wide the CTCF deposition sites in chicken lymphoid and erythroid cells subjected to the 4C analysis. A good correlation between the density of these sites and the level of 4C signals was observed for the anchors located in CpG islands. It is thus possible that CTCF contributes to the clustering of CpG islands revealed in our experiments. Using ChIP-Seq experimental procedure we have mapped genome-wide the CTCF deposition sites in chicken lymphoid and erythroid cells subjected to the 4C analysis. CTCF deposition sites in chicken lymphoid and erythroid (induced and non-induced) cells.

2014-03-01 | E-GEOD-51846 | biostudies-arrayexpress

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