ArticleCell cycle (Georgetown, Tex.)2017
p53 binding sites in normal and cancer cells are characterized by distinct chromatin context.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- EpGAT: integrating epigenetics and 3D genome structure to predict alternative splicing and polyadenylation.Briefings in bioinformatics · 2026Article
- Dissecting cross-lineage tumourigenesis under p53 inactivation through single-cell multi-omics and spatial transcriptomics.Clinical and translational medicine · 2025Article
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Article
- ChIP-DIP maps binding of hundreds of proteins to DNA simultaneously and identifies diverse gene regulatory elements.Nature genetics · 2024Article
- Chromatin structure related to oncogenesis.Cancer science · 2023Review
- Polymorphisms within DIO2 and GADD45A genes increase the risk of liver disease progression in chronic hepatitis b carriers.Scientific reports · 2023Article
- HERVs and Cancer-A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers.Biomedicines · 2023Review
- Activating STING1-dependent immune signaling inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.Free radical biology & medicine · 2021Review
- Widespread Exaptation of L1 Transposons for Transcription Factor Binding in Breast Cancer.International journal of molecular sciences · 2021Article
- Temporal gene regulation by p53 is associated with the rotational setting of its binding sites in nucleosomes.Cell cycle (Georgetown, Tex.) · 2021Article
- MOSTWAS: Multi-Omic Strategies for Transcriptome-Wide Association Studies.PLoS genetics · 2021Article
- Genomic retargeting of p53 and CTCF is associated with transcriptional changes during oncogenic HRas-induced transformation.Communications biology · 2020Article
- Single molecule studies reveal that p53 tetramers dynamically bind response elements containing one or two half sites.Scientific reports · 2020Article
- DNA Methylation Associated with Mitochondrial Dysfunction in a South African Autism Spectrum Disorder Cohort.Autism research : official journal of the International Society for Autism Research · 2020Article
- 2-[(4-Hydroxybenzyl) Amino] Phenol (HBAP) Restores the Mutated p53 to the Level Similar to That of Wild-Type p53 Protein and Inhibits Breast Cancer GrowthFrontiers in cell and developmental biology · 2020Article
- The Rich World of p53 DNA Binding Targets: The Role of DNA Structure.International journal of molecular sciences · 2019Review
- The nucleosome position-encoding WW/SS sequence pattern is depleted in mammalian genes relative to other eukaryotes.Nucleic acids research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor protein p53 interacts with DNA in a sequence-dependent manner. Thousands of p53 binding sites have been mapped genome-wide in normal and cancer cells. However, the way p53 selectively binds its cognate sites in different types of cells is not fully understood. Here, we performed a comprehensive analysis of 25 published p53 cistromes and identified 3,551 and 6,039 'high-confidence' binding sites in normal and cancer cells, respectively. Our analysis revealed 2 distinct epigenetic features underlying p53-DNA interactions in vivo. First, p53 binding sites are associated with transcriptionally active histone marks (H3K4me3 and H3K36me3) in normal-cell chromatin, but with repressive histone marks (H3K27me3) in cancer-cell chromatin. Second, p53 binding sites in cancer cells are characterized by a lower level of DNA methylation than their counterparts in normal cells, probably related to global hypomethylation in cancers. Intriguingly, regardless of the cell type, p53 sites are highly enriched in the endogenous retroviral elements of the ERV1 family, highlighting the importance of this repeat family in shaping the transcriptional network of p53. Moreover, the p53 sites exhibit an unusual combination of chromatin patterns: high nucleosome occupancy and, at the same time, high sensitivity to DNase I. Our results suggest that p53 can access its target sites in a chromatin environment that is non-permissive to most DNA-binding transcription factors, which may allow p53 to act as a pioneer transcription factor in the context of chromatin.
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