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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

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

Maternal inherited siRNA initiate piRNA cluster formation

Project description:Maternal inherited siRNA initiate piRNA cluster formation

| PRJNA794746 | ENA

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

ADAR1 regulates melanoma progression via miRNAs biogenesis

Project description:Aberrant RNA-editing was observed in several human tumors, but its significance is mostly unknown. Here we show that ADAR1, a ubiquitous RNA-editing enzyme, is commonly lost in metastatic melanoma cells and specimens. Experimental ADAR1 silencing significantly alters melanoma cell morphology, facilitates proliferation and cell-cycle, and increases the tumorigenicity in-vivo. A series of ADAR1 truncation mutants establishes a novel RNA-editing-independent role for ADAR1 in controlling the nuclear and cytoplasmic processing steps of miRNA biogenesis. Altered expression of ADAR1-controled miRNAs accounts for the observed phenotype. We show that the oncogenic miR-17-5p endogenously regulates ADAR1 expression and that its genomic sequence is frequently amplified in melanoma to overexpress the mature miR-17-5p form. ADAR1 and miR-17-5p are ubiquitously expressed, suggesting the generality of this mechanism. Melanoma cell line expressing low ADAR1 levels (ADAR1-Knockdown) using shRNA technique were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to examine the alterations in the genes and microRNA expression profile in the manipulated cell system, due to ADAR1 possible involvement cancer development. To that end, we selected ADAR1-knockdown (ADAR1-KD) cells that demonstrated an enhanced aggressive phenotype both in vivo and in vitro as compared to the control cells (Control).

2012-08-31 | E-GEOD-31963 | biostudies-arrayexpress

ADAR1-editing in HeLa, p150-KO and ADAR1-KO transcriptomes

Project description:RNAseq analysis of cell lines with ADAR1-p150 and ADAR1-p110 knock-outs and primary human tissue samples (from GSE57353 and GSE99392 data sets) to identify sites of ADAR1 editing

2018-12-04 | GSE115127 | GEO

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