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Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells

ABSTRACT: Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells

PROVIDER: PRJNA503859 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8158980_1.fastq.gz	Fastqsanger.gz
	SRR8158980_2.fastq.gz	Fastqsanger.gz
	SRR8158990_1.fastq.gz	Fastqsanger.gz
	SRR8158990_2.fastq.gz	Fastqsanger.gz
	SRR8158981_1.fastq.gz	Fastqsanger.gz

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Epigenetic therapy induces transcription of Inverted SINEs and ADAR1 dependency

Project description:In this study we show that intronic and intergenic SINE elements, specifically inverted repeats (IR) Alus, are the major source of drug-induced immunogenic dsRNA. These IR-Alus are frequently located downstream of ‘orphan’ CpG Islands (CGIs). In mammals, the enzyme Adenosine Deaminases Acting on RNA (ADAR1) targets and destabilizes IR-Alu dsRNA, which prevents activation of MDA5. We found that ADAR1 establishes a negative feedback loop, restricting the viral mimicry response to epigenetic therapy. Depletion of ADAR1 in patient-derived cancer cells potentiates the efficacy of epigenetic therapy, restraining tumour growth and reducing cancer initiation. Thus, epigenetic therapies trigger viral mimicry by inducing a subset of IR-Alus, leading to an ADAR1 dependency. Our findings suggest that combining epigenetic therapies with ADAR1 inhibitors represents a promising new strategy for cancer treatment.

2020-10-20 | GSE145639 | GEO

Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells.

Project description:Systematic exploration of cancer cell vulnerabilities can inform the development of novel cancer therapeutics. Here, through analysis of genome-scale loss-of-function datasets, we identify adenosine deaminase acting on RNA (ADAR or ADAR1) as an essential gene for the survival of a subset of cancer cell lines. ADAR1-dependent cell lines display increased expression of interferon-stimulated genes. Activation of type I interferon signaling in the context of ADAR1 deficiency can induce cell lethality in non-ADAR1-dependent cell lines. ADAR deletion causes activation of the double-stranded RNA sensor, protein kinase R (PKR). Disruption of PKR signaling, through inactivation of PKR or overexpression of either a wildtype or catalytically inactive mutant version of the p150 isoform of ADAR1, partially rescues cell lethality after ADAR1 loss, suggesting that both catalytic and non-enzymatic functions of ADAR1 may contribute to preventing PKR-mediated cell lethality. Together, these data nominate ADAR1 as a potential therapeutic target in a subset of cancers.

| S-EPMC6303303 | biostudies-literature

Circular RNA Expression is Suppressed by Androgen Receptor (AR) Regulated Adenosine DeAminase that act on RNA (ADAR1) in Human Hepatocellular Carcinoma

Project description:Hepatocellular carcinoma (HCC) is a heterogeneous malignancy as a result of complex genetic and epigenetic alterations. HCC is characterized by a clear gender disparity for which lacking a clear mechanistic understanding. By utilizing circular RNA (circRNA) microarray survey coupled with in vitro analysis, we analyzed the influence of androgen receptor (AR) on circRNA expression in HCC. Our results indicated that AR could suppress circRNA expression by up-regulating adenosine deaminase that act on RNA (ADAR1) p110 at a transcriptional level. Reporter assay further confirmed the role of AR as a transcriptional activator of ADAR1 expression. Furthermore, data collected from our center strongly suggest that ADAR1 expression can effectively predict HCC patients’ prognosis and an abnormal overexpression of ADAR1 is positively correlated with AR in HCC. In addition, we found CircARSP91 (hsa_circ_0085154), one of the circRNAs down-regulated by AR in an ADAR1-dependent manner, could inhibit HCC tumor growth both in vitro and in vivo. These findings highlight the fact that AR as a contributing factor for gender disparity in HCC can cause complex consequences though regulation of circRNA expression. Better understanding of roles of circRNA during HCC initiation and progression will be a key to develop novel HCC therapies.

2020-02-01 | GSE94520 | GEO

Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells

Project description:Using RNA-seq to identify gene expression changes after genetic deletion of ADAR

2018-11-06 | GSE122168 | 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

ADAR1 RNA editing quenches innate immune activation in endothelial cells

Project description:RNA editing has been shown to implicate in cardiovascular diseases, including dysregulated RNA editing in endothelial cell (EC) that involves Adenosine Deaminase Acting on RNA1 (ADAR1). However, the specific function of ADAR1 in EC at physiologic condition has not been established and the mechanism remains to be defined. This study is to determine the specific physiologic role of ADAR1 in EC and reveal its molecular and cellular mechanisms.

2021-12-27 | GSE174216 | GEO

RNA editing by ADAR1 leads to context-dependent transcriptome-wide changes in RNA Secondary Structure

Project description:Adenosine deaminase acting on RNA 1 (ADAR1) is the master RNA editor, catalyzing the deamination of adenosine to inosine. RNA editing is vital for preventing abnormal activation of cytosolic nucleic acid sensing pathways by self-double-stranded RNAs. Here we determine by parallel analysis of RNA secondary structure sequencing (PARS-seq), the global RNA secondary structure changes in ADAR1 deficient cells. Surprisingly, ADAR1 silencing resulted in a lower global double-stranded to single-stranded RNA ratio, suggesting that A-to-I editing can stabilize a large subset of imperfect RNA duplexes. The duplexes destabilized by editing are composed of vastly complementary inverted Alus found in untranslated regions of genes with vital biological processes, including housekeeping functions and type-I interferon responses. They are predominantly cytoplasmic and generally demonstrate higher ribosomal occupancy. Our findings imply that the editing effect on RNA secondary structure is context dependent and underline the intricate regulatory role of ADAR1 on global RNA secondary structure.

2017-06-25 | GSE100210 | GEO

Intact and native mass spectrometry analysis of human ADAR1 deaminase domain

Project description:Intact and native mass spectrometry analysis of human ADAR1 deaminase domain WT protein (hADAR1d WT) was carried out to support the finding of an additional metal-binding site.

2020-08-27 | MSV000086035 | MassIVE

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

2003-07-14 | GSE529 | GEO

ADAR1-dependent editing participates to the human beta-cells transcriptome diversity during inflammation

Project description:Enterovirus infection has long been suspected as a possible trigger for type 1 diabetes. Upon infection, viral double-stranded RNA (dsRNA) is recognized by membrane and cytosolic sensors that orchestrate the type I interferon signaling and the recruitment of innate immune cells to the pancreatic islets. In this context, adenosine deaminase acting on RNA 1 (ADAR1) editing plays an important role in dampening the immune response by inducing adenosine mispairing, destabilizing the RNA duplexes and thus preventing an excessive immune activation. Here, we evaluated the role of ADAR1 in human pancreatic b cells and determined the impact of type 1 diabetes pathophysiological environment on ADAR1-dependent RNA editing. We show that both IFNα or IFNɣ/IL1β stimulation promotes ADAR1 expression and increases the A-to-I RNA editing of Alu-Containing mRNAs in EndoC-bH1 cells as well as primary human islets. We demonstrate that ADAR1 overexpression inhibits the type I interferon response signaling, while ADAR1 silencing potentiates IFNα effects. In addition, ADAR1 overexpression triggers the generation of alternative spliced RNAs, highlighting a novel role for ADAR1 as regulator of the b cell transcriptome under inflammatory conditions.

2022-11-23 | GSE214851 | GEO

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