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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

ABSTRACT: Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

PROVIDER: PRJNA915218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22873649_1.fastq.gz	Fastqsanger.gz
	SRR22873649_2.fastq.gz	Fastqsanger.gz
	SRR22873650_1.fastq.gz	Fastqsanger.gz
	SRR22873650_2.fastq.gz	Fastqsanger.gz
	SRR22873651_1.fastq.gz	Fastqsanger.gz

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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

Project description:Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

| PRJNA915215 | ENA

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

Project description:Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

| PRJNA915219 | ENA

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

Project description:RNAseq of Adult Liver in ADAR1 E861A, ADARp110, ADAR p150, ADAR1 knock in mice generated by deep sequencing.

2023-04-28 | GSE221626 | GEO

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

Project description:RNAseq of Osteosarcoma model from ADAR1 knock in mice generated by deep sequencing.

2023-04-28 | GSE221627 | GEO

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

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

2023-04-26 | GSE221628 | GEO

Microrna expression profile in ADAR1 p110 overexpression

Project description:The change in Microrna expression profile in ADAR1 p110 overexpression.

2022-03-31 | E-MTAB-11574 | biostudies-arrayexpress

Over-expression of ADAR1 in mice does not initiate or accelerate cancer formation <i>in vivo</i>.

Project description:Adenosine to inosine editing (A-to-I) in regions of double stranded RNA (dsRNA) is mediated by adenosine deaminase acting on RNA 1 (ADAR1) or ADAR2. ADAR1 and A-to-I editing levels are increased in many human cancers. Inhibition of ADAR1 has emerged as a high priority oncology target, however, whether ADAR1 overexpression enables cancer initiation or progression has not been directly tested. We established a series of in vivo models to allow overexpression of full-length ADAR1, or its individual isoforms, to test if increased ADAR1 expression was oncogenic. Widespread over-expression of ADAR1 or the p110 or p150 isoforms individually as sole lesions was well tolerated and did not result in cancer initiation. Therefore, ADAR1 overexpression alone is not sufficient to initiate cancer. We demonstrate that endogenous ADAR1 and A-to-I editing increased upon immortalization in murine cells, consistent with the observations from human cancers. We tested if ADAR1 over-expression could co-operate with cancer initiated by loss of tumour suppressors using a model of osteosarcoma. We did not see a disease potentiating or modifying effect of overexpressing ADAR1 or its isoforms in the models assessed. We conclude that increased ADAR1 expression and A-to-I editing in cancers is most likely a consequence of tumor formation.

| S-EPMC10233902 | biostudies-literature

ADAR1 overexpression in MDA-MB-231 cells

Project description:ADAR1 overexpression in MDA-MB-231 cells

| PRJNA547525 | ENA

Gene Amplification Associated Overexpression of the RNA Editing Enzyme ADAR1 Enhances Human Lung Tumorigenesis

Project description:The introduction of new therapies against particular genetic mutations in non-small cell lung cancer is a promising avenue for improving the survival of these patients, but the target population is small. There is a need to uncover new potential actionable genetic lesions and non-conventional cancer pathways, such as RNA editing, are worthy to explore. Herein we show that the adenosine-to-inosine editing enzyme ADAR1 undergoes gene amplification in non-small cancer cell lines and primary tumors in association with higher levels of the corresponding mRNA and protein. From a growth and invasion standpoint, the depletion of ADAR1 expression in amplified cells reduces their tumorigenic potential in cell culture and mice models, whereas its overexpression causes the opposite effects. From a functional perspective, ADAR1 overexpression enhances the editing frequencies of target transcripts such as NEIL1 and miR-381. In the clinical setting, patients with early stage lung cancer, but harboring ADAR1 gene amplification, show poor outcome. Overall, our results indicate a role for ADAR1 as a lung cancer oncogene undergoing gene amplification-associated activation that affect downstream RNA editing patterns and patient prognosis.

2018-04-08 | GSE67660 | GEO

ADAR1 regulates dsRNA formation in nuclear and mitochondrial transcripts through editing-dependent and -independent mechanisms

Project description:Endogenous (self) double-stranded RNAs (dsRNAs) in human cells can activate innate immune responses. ADAR1, an A-to-I editing enzyme of dsRNAs, suppresses aberrant immune activation by self-dsRNAs. However, how ADAR1 influences the cellular dsRNA landscape remains unclear. We show that human ADAR1 downregulates self-dsRNA abundance through editing-dependent and editing-independent mechanisms. We further conducted quantitative dsRNA-sequencing on wild-type and ADAR1-deficient cells. dsRNAs are enriched in protein-coding mRNAs − especially those with repetitive elements and elongated 3’UTRs − and mitochondrial RNAs. ADAR1 loss markedly increased dsRNA quantity but minimally impacted dsRNA identity. ADAR1-regulated dsRNA transcripts consist of nuclear-encoded mRNAs and, unexpectedly, mitochondria-encoded RNAs rarely edited by ADAR1. Accordingly, dsRNAs accumulate to high levels within the mitochondria of ADAR1-deficient cells. Notably, ADAR1 loss sensitizes cells to inflammation under mitochondrial stress (e.g., mitochondrial herniation, X-ray radiation). Hence, we show that dsRNAs regulated by ADAR1 go beyond A-to-I edited transcripts, and that ADAR1 can control mitochondrial-dsRNAs.

2026-01-13 | GSE293278 | GEO

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