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KMID : 0620920230550010095
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Experimental & Molecular Medicine
2023 Volume.55 No. 1 p.95 ~ p.107
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ADAR1-dependent miR-3144-3p editing simultaneously induces MSI2 expression and suppresses SLC38A4 expression in liver cancer
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Kim Hyung-Seok
Na Min-Jeong
Son Keun-Hong
Yang Hee-Doo
Kim Sang-Yean
Shin Eun-Bi
Ha Jin-Woong
Jeon So-Young
Kang Keun-Soo
Moon Ki-Ho
Park Won-Sang
Nam Suk-Woo
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Abstract
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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?
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