| Autor: |
Hyung Seok Kim, Min Jeong Na, Keun Hong Son, Hee Doo Yang, Sang Yean Kim, Eunbi Shin, Jin Woong Ha, Soyoung Jeon, Keunsoo Kang, Kiho Moon, Won Sang Park, Suk Woo Nam |
| Rok vydání: |
2023 |
| Předmět: |
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| Zdroj: |
Experimental & Molecular Medicine. 55:95-107 |
| ISSN: |
2092-6413 |
| DOI: |
10.1038/s12276-022-00916-8 |
| Popis: |
Aberrant adenosine-to-inosine (A-to-I) RNA editing, catalyzed by adenosine deaminase acting on double-stranded RNA (ADAR), has been implicated in various cancers, but the mechanisms by which microRNA (miRNA) editing contributes to cancer development are largely unknown. Our multistage hepatocellular carcinogenesis transcriptome data analyses, together with publicly available data, indicated that ADAR1 was the most profoundly dysregulated gene among RNA-editing enzyme family members in liver cancer. Targeted inactivation of ADAR1 inhibited the in vitro tumorigenesis of liver cancer cells. An integrative computational analyses of RNA-edited hotspots and the known editing frequency of miRNAs suggested that the miRNA miR-3144-3p was edited by ADAR1 during liver cancer progression. Specifically, ADAR1 promoted A-to-I editing of canonical miR-3144-3p to replace the adenosine at Position 3 in the seed region with a guanine (ED_miR-3144-3p(3_A Musashi RNA-binding protein 2 (MSI2) was a specific target of miR-3144-3p and that MSI2 overexpression was due to excessive ADAR1-dependent over-editing of canonical miR-3144-3p in liver cancer. In addition, target prediction analyses and validation experiments identified solute carrier family 38 member 4 (SLC38A4) as a specific gene target of ED_miR-3144-3p(3_A |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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