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

ABSTRACT: 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 significally expressed by DNA damage and and are non- coding. HCT116 p53 wt cell transfected with the ASO-SC, ASO lncRNA-1 and ASO unassigned-1 for depletion of this new lncRNAs and treated with the DNA damage drug 5FU for 12h were analyzed in the affimetrix platform HTA2.

ORGANISM(S): Homo sapiens

SUBMITTER: Maite Huarte

PROVIDER: E-GEOD-58409 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

PINT lincRNA connects the p53 pathway with epigenetic silencing by the Polycomb Repressive Complex 2 (MEF cells)

Project description:It has been recently shown that the transcription factor p53 induces the expression of multiple lincRNAs. However, relatively little is known about the role that lincRNAs play in this pathway. Here we characterize a lincRNA named PINT (p53 Induced Noncoding Transcript). We show that PINT is a ubiquitously expressed lincRNA that is finely regulated by p53. In mouse cells, PINT promotes cell proliferation and survival by regulating the expression of genes of TGF-beta, MAPK and p53 pathways. PINT is a nuclear lincRNA that directly interacts with Polycomb Repressive Complex 2 (PRC2), being required for PRC2 targeting of specific genes for repression. Furthermore, PINT functional activity is dependent on PRC2 expression, representing a connection between the p53 pathway and epigenetic regulation by PRC2. We have also identified PINT human ortholog (hPINT), which presents suggestive analogies with the mouse lincRNA. hPINT is similarly regulated by p53, and its expression correlates significantly with the same cellular pathways as the mouse ortholog, including the p53 pathway. Interestingly, hPINT is significantly downregulated in colon cancer, representing a novel tumor suppressor candidate. Our results not only help our understanding of the role of p53 and lincRNAs in cancer, but also contribute to the open debate regarding the utility of mouse models for the study of lincRNAs. Inhibition of PINT or p53 gene expression and subsequent treatment with 150 nM doxorubicine for 12h in MEF LSL p53 +/+ cells.

2013-08-09 | E-GEOD-46247 | biostudies-arrayexpress

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

2014-12-22 | GSE58409 | GEO

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

2014-12-22 | GSE58507 | GEO

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

2014-12-22 | GSE58506 | GEO

A long noncoding RNA regulates sister chromatid cohesion [RNA-seq]

Project description:Long noncoding RNAs (lncRNAs) have appeared to be involved in the most diverse cellular processes through multiple mechanisms. Here we describe a previously uncharacterized human lncRNA, CONCR (cohesion regulator noncoding RNA), transcriptionally activated by MYC, which is upregulated in multiple cancer types. The expression of CONCR is cell cycle-regulated, and it is required for cell cycle progression and DNA replication. Moreover, cells depleted of CONCR show severe defects in sister chromatid cohesion, suggesting an essential role for CONCR in cohesion establishment during cell division. CONCR interacts with and regulates the activity of DDX11, a DNA-dependent ATPase and helicase involved in DNA replication. These findings suggest a novel mechanism of action for CONCR in the modulation of DDX11 enzymatic activity, unveiling the direct involvement of a lncRNA in the establishment of sister chromatid cohesion. Characterization of the function of the long noncoding RNA CONCR. HCT116 p53-/- cells were left untreated (0h) or treated with the DNA damaging drug 5-FU for 4h and 12h.

2016-08-03 | E-GEOD-81601 | biostudies-arrayexpress

p53-dependent regulation of gene expression following DNA damage

Project description:Long noncoding RNAs (lncRNAs) are prevalent genes with frequently exquisite regulation but mostly unknown functions. Here we demonstrate a role of lncRNAs in guiding signal transduction. DNA damage activates transcription of DINO (Damage Induced NOncoding) via p53. DINO knockdown blocks DNA damage-induced gene expression and cell cycle arrest. Conversely, enforced expression of DINO activates damage signaling without DNA damage. DINO binds p53 and selectively promotes SET7 methylation of p53 at lysine 372 over other substrates, which stabilizes p53 in an auto-amplification loop. Our results suggest that inducible lncRNA can achieve catalysis-like effects to rewire cellular signaling networks. RNA was isolated from human fetal lung fibroblasts, HCT116 p53+/+, or HCT116 p53-/- cells treated with doxorubicin or sham for 26 hours. Human fetal lung fibroblasts were transfected with siRNAs targeting DINO or non-targeting control and subsequently treated with doxorubicin for 26 hours.

2012-11-20 | E-GEOD-42368 | biostudies-arrayexpress

Effect of wtp53-reactivating drug RITA on HCT116 cells

Project description:Since its discovery as a tumour suppressor some fifteen years ago, the transcription factor p53 has attracted paramount attention for its role as “the guardian of the genome”. TP53 mutations occur so frequently in cancer, regardless of patient age or tumour type, that they appear to be part of the life history of at least 50% of human tumours. In most tumours that retain wild-type p53, its function is inactivated due to deregulated HDM2, a protein which binds to p53 and which can inhibit the transcriptional activity of p53 and induce its degradation. RITA is a low-molecular-weight compound which addresses the second group of tumours retaining functionally reactive wt p53. It was found in a screening of the National Cancer Institute (NCI) library of low-molecular-weight compounds based on its ability to selectively kill wtp53-containing cells. RITA binds directly to p53 and diplaces its main destructor Mdm2, as well as inducing a shift in the conformation of p53. This is in contrast to the wtp53-reactivating compound Nutlin3a, which targets Mdm2, inhibiting its ability to degrade p53. Using microarray technology we have explored the effect of RITA on the transcriptome of isogenic cell-lines with knocked-out (KO) or intact (WT) TP53. While the effects on KO cells are below detection limit, the effects on WT cells are profound. The known p53 targets induced are predominately apoptotic, in contrast to the genes affected by Nutlin3a, which are exclusively growth-arrest genes. Keywords: Antitumor agent HCT116 parental and HCT116 p53-null (HCT116 TP53-/-) cells were subjected to treatment with 1uM RITA for 12h, or left untreated. The experiment was done in three independent biological replicates.

2009-02-28 | E-GEOD-11578 | biostudies-arrayexpress

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

Gene expression profiling of CYC116 and ZM447439 resistant HCT116 wild type and HCT116 p53 null clones in comparison to parent cell lines

Project description:HCT116 and HCT116 p53 null were exposed to two Aurora kinase inhibitors (CYC116 and ZM447439) at cytotoxic concentrations. Within 4-5 weeks we were able to select and isolate 10 drug resistant clones from each group. 3 clones were selected for gene expression profiling using Affymetrix microarrays (Human Gene 1.0 ST Array). The samples in each group were initially given the code names as follows. Group 1. [R1.3, R4.2, R6.3: CYC116 p53 wild type], Group 2. [R8.7, R9.7, R10.7:CYC116 p53 null], Group 3. [R7.1, R15.1, R16.1:ZM447439 p53 wild type], and Group 4. [R1.5, R3.5, R4.5:ZM447439 p53 null). For publication purpose the names were later changed to, Group 1. [R1.1, R1.2, R1.3: CYC116 p53 wild type], Group 2. [R2.1, R2.2, R2.3:CYC116 p53 null], Group 3. [R3.1, R3.2, R3.3:ZM447439 p53 wild type], and Group 4. [R4.1, R4.2, R4.3:ZM447439 p53 null].

2012-04-01 | E-MEXP-3526 | biostudies-arrayexpress

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