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ADAR1 may be involved in the proliferation of acute myeloid leukemia cells via regulation of the Wnt pathway

Authors Xiao H, Cheng Q, Wu X, Tang Y, Liu J, Li X

Received 29 March 2019

Accepted for publication 12 August 2019

Published 20 September 2019 Volume 2019:11 Pages 8547—8555

DOI https://doi.org/10.2147/CMAR.S210504

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Xueqiong Zhu


Han Xiao, Qian Cheng, Xinyu Wu, Yishu Tang, Jing Liu, Xin Li

Department of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People’s Republic of China

Correspondence: Xin Li; Jing Liu
Department of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People’s Republic of China
Tel/fax +86 7 318 861 8014
Email lixiner1975@163.com; lj0jingliu@163.com

Purpose: Acute myeloid leukemia (AML) is the most common type of leukemia and characterized by the malignant growth of leukemic cells. Adenosine deaminases acting on RNA 1 (ADAR1) have been shown to participate in the proliferation of cancer cells and progression of various cancers. However, the role of ADAR1 in AML has not been investigated.
Patients and methods: We compared the expression levels of ADAR1 between samples obtained from different AML patients and controls using quantitative-polymerase chain reaction and Western blotting. We also investigated the functional role and possible mechanisms via silencing the expression of ADAR1 in vitro and in vivo.
Results: We found that the mRNA and protein levels of ADAR1 were significantly higher in AML patients. The mRNA expression of ADAR1 was positively correlated with the ratio of leukemic cells. Additionally, silencing of ADAR1 expression significantly suppressed the proliferation of AML cells and induced G0/1 arrest. For the analysis of the mechanism, the quantitative-polymerase chain reaction and Western blotting results revealed that ADAR1 knockdown resulted in the decreased expression of Wingless-Int (Wnt) effectors including β-catenin, c-Myc, transcription factor 4, and cyclin D2. In the nude mouse model, inhibition of ADAR1 expression reduced the tumorigenic potential and decreased the expression o]f Wnt effectors.
Conclusion: These results demonstrate that ADAR1 may be involved in the regulation of the proliferation of AML cells partially via regulation of the Wnt signaling pathway.

Keywords: acute myeloid leukemia, ADAR1, proliferation, cell cycle, Wnt pathway

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