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Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

ABSTRACT: Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

PROVIDER: PRJNA507260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8249170_1.fastq.gz	Fastqsanger.gz
	SRR8249170_2.fastq.gz	Fastqsanger.gz
	SRR8249171_1.fastq.gz	Fastqsanger.gz
	SRR8249171_2.fastq.gz	Fastqsanger.gz
	SRR8249172_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported that aberrant A-to-I RNA editing profiles are implicated in cancers. Albeit changes in expression and activity of ADAR genes are thought to have been responsible for the dysregulated RNA editome in diseases, they are not always correlated, indicating the involvement of secondary regulators. Here, we uncover DAP3 as a potent repressor of editing and a strong oncogene in cancer. DAP3 mainly interacts with the deaminase domain of ADAR2 and represses editing via disrupting association of ADAR2 with its target transcripts. PDZD7, an exemplary DAP3-repressed editing target, undergoes a protein recoding editing at stop codon [Stop →Trp (W)]. Because of editing suppression by DAP3, the unedited PDZD7WT, which is more tumorigenic than edited PDZD7Stop518W, is accumulated in tumors. In sum, cancer cells may acquire malignant properties for their survival advantage through suppressing RNA editome by DAP3.

2020-06-23 | GSE123020 | GEO

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression.

| S-EPMC7299630 | biostudies-literature

Bidirectional regulation of adenosine-to-inosine (A-to-I) RNA editing by DEAH box helicase 9 (DHX9) in cancer

Project description:Adenosine-to-inosine (A-to-I) RNA editing entails the enzymatic deamination of adenosines to inosines by adenosine deaminases acting on RNA (ADARs). Dysregulated A-to-I editing has been implicated in various diseases, including cancers. However, the precise factors governing the A-to-I editing and their physiopathological implications remain as a long-standing question. Herein, we unravel that DEAH box helicase 9 (DHX9), at least partially dependent of its helicase activity, functions as a bidirectional regulator of A-to-I editing in cancer cells. Intriguingly, the ADAR substrate specificity determines the opposing effects of DHX9 on editing as DHX9 silencing preferentially represses editing of ADAR1-specific substrates, whereas augments ADAR2-specific substrate editing. Analysis of 11 cancer types from The Cancer Genome Atlas (TCGA) reveals a striking overexpression of DHX9 in tumors. Further, tumorigenicity studies demonstrate a helicase-dependent oncogenic role of DHX9 in cancer development. In sum, DHX9 constitutes a bidirectional regulatory mode in A-to-I editing, which is in part responsible for the dysregulated editome profile in cancer.

2018-05-31 | GSE99789 | GEO

Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

Project description:The dynamic regulation of transcriptome requires coordinated participation of multiple RNA binding proteins (RBPs) in RNA processing. Dysregulated RNA processing, such as aberrant alternative splicing, is implicated in many cancers. Therefore, it is critical to explore the cancer-related RNA processing regulation and the underlying mechanisms. Many RBPs lack classical RNA-binding domains and their functions in RNA processing regulation remain unclear. Through an unbiased transcriptome-wide analysis, we report DAP3 binds ubiquitously to endogenous RNAs in vivo and its depletion reshapes the alternative splicing landscape in cancer cells. Mechanistically, we show DAP3 coordinates splicing regulatory networks, not only via mediating the formation of ribonucleoprotein (RNP) complexes, but also via modulating splicing of numerous splicing factors. Specific DAP3-regulated splicing changes such as non-productive splicing of WSB1 and RBM6, play important roles in tumorigenesis. Together, these findings provide critical mechanistic insights into the molecular functions of DAP3 in cancer development as a master regulator of RNA processing.

2022-02-10 | GSE172078 | GEO

Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

Project description:Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

| PRJNA994439 | ENA

Testicular adenosine to inosine RNA editing in the mouse

Project description:Adenosine to inosine (A-to-I) RNA editing occurs in a wide range of tissues and cell types and can be catalyzed by one of two adenosine deaminase acting on double stranded RNA enzymes, ADAR and ADARB1. Editing can impact both coding and non-coding regions of RNA, and in higher organisms, has been proposed to function in adaptive evolution. Neither the prevalence of A-to-I editing nor the role of either ADAR or ADARB1 has been examined in the context of germ cell development in mammals. Computational analysis of whole testis and cell type specific RNA-sequencing data followed by molecular confirmation demonstrated that A-to-I RNA editing occurs in both the germ line and in somatic Sertoli cells in two targets, Cog3 and Rpa1. Expression analysis demonstrated both Adar and Adarb1 were expressed in both Sertoli cells and in a cell-type dependent manner during germ cell development. Conditional ablation of Adar did not impact testicular RNA editing in either germ cells or Sertoli cells. Additionally, Adar ablation in either cell type did not have gross impacts on germ cell development or male fertility. In contrast, global Adarb1 knockout animals demonstrated a complete loss of A-to-I RNA editing in spite of normal germ cell development. Taken together, these observations demonstrate ADARB1 mediates A-to-I RNA editing in the testis and these editing events are dispensable for male fertility in an inbred mouse strain in the lab.

2016-12-24 | GSE92870 | GEO

Determine the ADAR1 editome during IFN response.

Project description:ADAR1 is an interferon (IFN) inducible RNA editing enzyme that converts adenosine (A) to inosine (I). Here we identified ADAR1 and ADAR1p150 specific editing events by conducting RNA-seq on WT, ADAR1 KO, and ADAR1p150 KO cells.

2018-02-09 | GSE99249 | GEO

Discovery of DAP3-binding RNA sites by eCLIP

Project description:eCLIP paired-end sequencing of DAP3 in EC109 cells with two biological replicates. This analysis revealed the genome-wide RNA binding landscape of DAP3, as the supporting data of the main publication.

2020-06-23 | GSE144318 | GEO

The C. elegans neural editome reveals an ADAR target mRNA required for proper chemotaxis

Project description:ADAR proteins alter gene expression both via catalyzing adenosine-to-inosine RNA editing and in an editing-independent manner by binding to target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. To identify important neuronal targets in C. elegans, we performed the first unbiased assessment of the effects of ADR-2, the C. elegans editing enzyme, on the neural transcriptome. We identified the neural editome and gene expression changes associated with the loss of adr-2. As C. elegans lacking adr-2 exhibit reduced chemotaxis, our studies focused on targets that regulate this process. We identified an edited mRNA, clec-41, whose expression is dependent on ADR-2. Expressing clec-41 in adr-2 deficient neural cells restored chemotaxis. This study is the first of its kind in the RNA editing field to span from developing novel methodology for tissue-specific target identification to organismal behavior, significantly advancing our understanding of ADAR functions in neural cells.

2017-06-13 | GSE98869 | GEO

New targets of Drosophila adenosine deaminase acting on RNA (dADAR)

Project description:The aim of this experiment is to identify new targets of Drosophila adenosine deaminase acting on RNA (dADAR) by enriching Inosine-containing mRNA (I-mRNA) from wild type (C-S) and dADAR mutant flies and then hybridization with Drosophila cDNA arrays.

2010-06-05 | E-GEOD-529 | biostudies-arrayexpress

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