| Autor: |
Suk Woo Nam, 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 |
| Rok vydání: |
2022 |
| DOI: |
10.21203/rs.3.rs-1999877/v1 |
| Popis: |
Aberrant adenosine-to-inosine (A-to-I) RNA editing, catalyzed by adenosine deaminase acting on double-stranded RNA (ADAR), is implicated in various cancers, but the mechanisms by which microRNA (miRNA) editing contributes to cancer development are currently largely unknown. Our multi-step hepatocellular carcinogenesis transcriptome data analyses, together with publicly available data, indicated that ADAR1 is the most dysregulated gene among the RNA editing enzyme families in liver cancer. Targeted inactivation of ADAR1 inhibits in vitro tumorigenesis of liver cancer cells. Integrative computational analyses of RNA editing hotspots and the editing frequency of miRNAs suggested miR-3144-3p a potential mRNA edited by ADAR1 in liver cancer progression. ADAR1 promoted A-to-I editing of the canonical miR-3144-3p to change position 3 adenosine in the seed region to guanine (ED_miR-3144-3p(3_A Musashi RNA-binding protein 2 (MSI2) is a specific target of miR-3144-3p, and that MSI2 overexpression is due to ADAR1-dependent over-editing of the canonical miR-3144-3p in liver cancer. In addition, target prediction analyses and validation experiments identified solute carrier family 38 member 4 (SLC38A4) as specific target gene for ED_miR-3144-3p(3_A |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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