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Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells

ABSTRACT: Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells

OTHER RELATED OMICS DATASETS IN: E-GEOD-46493

PROVIDER: PRJNA201484 | ENA |

REPOSITORIES: ENA

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Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (Affymetrix)

Project description:The effects of diverse stresses on promoter selectivity and transcription regulation by the tumor suppressor p53 are poorly understood. We have taken a comprehensive approach to characterizing the human p53 network that includes p53 levels, binding, expression and chromatin changes under diverse stresses. Human osteosarcoma U2OS cells treated with anti-cancer drugs Doxorubicin or Nutlin-3 led to strikingly different p53 gene binding patterns based on ChIP-seq experiments. While two contiguous RRRCWWGYYY decamers is the consensus binding motif, p53 can bind a single decamer and function in vivo. Although the number of sites bound by p53 was 6-times greater for Nutlin-3 than Doxorubicin, expression changes induced by Nutlin-3 were much less dramatic compared to Doxorubicin. Unexpectedly, the solvent DMSO alone induced p53 binding to many sites common to Doxorubicin; however, this binding had no effect on target gene expression. Together, these data imply a two-stage mechanism for p53 transactivation where p53 binding only constitutes the first stage. Furthermore, both p53 binding and transactivation were associated with increased active histone modification H3K4me3. We discovered 149 putative new p53 target genes including several that are relevant to tumor suppression, revealing potential new targets for cancer therapy and expanding our understanding of the p53 regulatory network. Gene expression analysis (using Affymetrix Human Genome U133 Plus 2.0 GeneChipÂ® arrays) of the p53 response in U2OS cells treated with either Doxorubicin or Nutlin-3, relative to their controls No Treatment and DMSO, respectively.

2013-07-01 | E-GEOD-46493 | biostudies-arrayexpress

Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (Affymetrix)

2013-07-01 | GSE46493 | GEO

Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (ChIP-seq)

2013-07-01 | GSE46641 | GEO

E-GEOD-46493

Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (Affymetrix)

2015-07-13 | E-GEOD-46493 | ExpressionAtlas

Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells.

Project description: Not available

| S-EPMC3753631 | biostudies-literature

Homo sapiens

Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (Affymetrix)

| PRJNA200647 | ENA

Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-01 | E-GEOD-46642 | biostudies-arrayexpress

Homo sapiens

Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (ChIP-seq)

| PRJNA201486 | ENA

Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-07-01 | GSE46642 | GEO

Impact of transcriptional mutagenesis on p53 transactivation

Project description:The transcriptional error rate can be significantly increased by the presence of DNA lesions that instruct mis-insertion during transcription; a process referred to as transcriptional mutagenesis (TM). Herein, we determined the effect of O6-methylguanine (O6-meG) on transcription and subsequent transactivation activity of p53 in human lung H1299 cells. Levels of TM and effects on transactivation were determined by RNA-seq. Results showed that 47% of all p53 transcripts contained an uridine misincorporation opposite the lesion at 6 h post transfection, which was decreased to 18% at 24 h. TM at these levels reduced DNA binding activity of p53 to 21% and 80% compared to wild type p53, respectively. Gene expression data were analyzed to identify differentially expressed genes due to TM compared to the response of wild type p53. We show a temporal repression of transactivation of >100 high confidence p53 target genes including regulators of the cell cycle, DNA damage response and apoptosis. In addition, TM repressed the transcriptional downregulation by p53 of several negative regulators of proliferation and differentiation . Our work demonstrates that TM, even when restricting its effect to an individual transcription factor, has the potential to alter gene expression programs and diversify cellular phenotypes.

2019-10-16 | GSE138853 | GEO

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