Mol. Cells 2023; 46(6): 351-359
Published online March 16, 2023
https://doi.org/10.14348/molcells.2023.2174
© The Korean Society for Molecular and Cellular Biology
Correspondence to : suhwan.chang@amc.seoul.kr
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
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.
Keywords ADAR1, ARPIN, breast cancer, metastasis, RNA editing
Mol. Cells 2023; 46(6): 351-359
Published online June 30, 2023 https://doi.org/10.14348/molcells.2023.2174
Copyright © The Korean Society for Molecular and Cellular Biology.
Min Ji Park1 , Eunji Jeong1
, Eun Ji Lee1
, Hyeon Ji Choi1
, Bo Hyun Moon2
, Keunsoo Kang3
, and Suhwan Chang1,4,*
1Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea, 2Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea, 3Department of Microbiology, College of Science & Technology, Dankook University, Cheonan 31116, Korea, 4Department of Physiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea
Correspondence to:suhwan.chang@amc.seoul.kr
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
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.
Keywords: ADAR1, ARPIN, breast cancer, metastasis, RNA editing
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