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Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq II)

ABSTRACT: The goal of our study is to investigate the role of the p53-induced lncRNA PURPL in the context of liver cancer. To achieve this, we identified transcript variants of PURPL expressed in liver cancer cells and assayed for the transcriptome changes caused by PURPL knockdown after p53 induction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206699 | GEO | 2022/10/18

REPOSITORIES: GEO

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Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (Iso-Seq)

Project description:The goal of our study is to investigate the role of the p53-induced lncRNA PURPL in the context of liver cancer. To achieve this, we identified transcript variants of PURPL expressed in liver cancer cells and assayed for the transcriptome changes caused by PURPL knockdown after p53 induction.

2022-10-18 | GSE206701 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq I)

2022-10-18 | GSE206698 | GEO

Identification of PURPL regulated genes in HCT116 cells

Project description:Analysis of changes in gene expression profile upon depletion of PURPL in HCT116 cells. The hypothesis in this study is that PURPL regulates gene expression in the p53 pathway.

2017-08-03 | GSE79053 | GEO

Mass spectrometry (MS) datasets of PURPL RNA pulldown samples in A375 cells

Project description:We performed PURPL RNA pulldown followed by MS analysis to identify purpl-interacting proteins in A375 cells.With high performance liquid chromatography-mass spectrometry (HPLC-MS), the binding protein of PURPL from RNA pull down was detected by removing non-specific protein which were binding with EGFP.

2022-02-16 | PXD028863 | Pride

PURPL Represses Radiation-induced Apoptosis to Promote Radioresistance in Cutaneous Melanoma by Direct Interfering with BID Cleavage

Project description:During the treatment of cutaneous melanoma, the presence of radioresistance compromised the therapeutic effects of radiotherapy. Yet, the mechanism of radioresistance in melanoma still remains unclear. Bioinformatic analysis of the transcriptomic sequencing showed PURPL was top up-regulated genes in response to ionizing radiation (IR) treatment in melanoma cells. Loss of PURPL notably repressed melanoma cell viability, colony formation, migration and invasiveness which potentiated PURPL’s role in radioresistance of melanoma. Further, loss-of- and gain-of-function analysis indicated that PURPL repressed IR-induced DNA damage and apoptosis. Mechanistically, RNA pulldown was performed and BID was identified as the interacting protein partner of PURPL. As the core gene of the mitochondrial apoptosis pathway, BID could be cleaved by Caspase-8 to generate tBID, which promotes the permeability of the mitochondrial membrane and the release of cytochrome c. IR treatment promotes the interaction between BID and Caspase-8 which was further strengthened by the loss of PURPL. The in vivo assays further verified the in vitro findings. Collectively, our study supports the pro-radioresistance role of PURPL in melanoma by inhibiting the interaction between BID and Caspase-8, which may provide a novel target for clinical radiotherapy.

2024-01-01 | GSE248024 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation

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

2022-10-18 | GSE206702 | GEO

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer.

Project description:Basal p53 levels are tightly suppressed under normal conditions. Disrupting this regulation results in elevated p53 levels to induce cell cycle arrest, apoptosis, and tumor suppression. Here, we report the suppression of basal p53 levels by a nuclear, p53-regulated long noncoding RNA that we termed PURPL (p53 upregulated regulator of p53 levels). Targeted depletion of PURPL in colorectal cancer cells results in elevated basal p53 levels and induces growth defects in cell culture and in mouse xenografts. PURPL associates with MYBBP1A, a protein that binds to and stabilizes p53, and inhibits the formation of the p53-MYBBP1A complex. In the absence of PURPL, MYBBP1A interacts with and stabilizes p53. Silencing MYBBP1A significantly rescues basal p53 levels and proliferation in PURPL-deficient cells, suggesting that MYBBP1A mediates the effect of PURPL in regulating p53. These results reveal a p53-PURPL auto-regulatory feedback loop and demonstrate a role for PURPL in maintaining basal p53 levels.

| S-EPMC5777516 | biostudies-literature

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

Project description:These studies characterized R273C-p53 and R273H-p53 in prostate cancer cells

2021-12-23 | GSE157336 | GEO

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

Project description:These studies characterized R273C-p53 and R273H-p53 in prostate cancer cells

2021-12-23 | GSE157335 | GEO

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

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