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자료유형
학술저널
저자정보
장수환 (울산대학교) Min Ji Park (Asan Medical Center University of Ulsan College of Medicine) Eunji Jeong (Asan Medical Center University of Ulsan College of Medicine) Eun Ji Lee (Asan Medical Center University of Ulsan College of Medicine) Hyeon Ji Choi (Asan Medical Center University of Ulsan College of Medicine) Bo Hyun Moon (Asan Medical Center University of Ulsan College of Medicine) Keunsoo Kang (Department of Microbiology College of Science & Technology Dankook University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제46권 제6호
발행연도
2023.6
수록면
351 - 359 (9page)
DOI
10.14348/molcells.2023.2174

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Deamination of adenine or cytosine in RNA, called RNA editing, is a constitutively active and common modification. The primary role of RNA editing is tagging RNA right after its synthesis so that the endogenous RNA is recognized as self and distinguished from exogenous RNA, such as viral RNA. In addition to this primary function, the direct or indirect effects on gene expression can be utilized in cancer where a high level of RNA editing activity persists. This report identified actin-related protein 2/3 complex inhibitor (ARPIN) as a target of ADAR1 in breast cancer cells. Our comparative RNA sequencing analysis in MCF7 cells revealed that the expression of ARPIN was decreased upon ADAR1 depletion with altered editing on its 3’UTR. However, the expression changes of ARPIN were not dependent on 3’UTR editing but relied on three microRNAs acting on ARPIN. As a result, we found that the migration and invasion of cancer cells were profoundly increased by ADAR1 depletion, and this cellular phenotype was reversed by the exogenous ARPIN expression. Altogether, our data suggest that ADAR1 suppresses breast cancer cell mobility via the upregulation of ARPIN.

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