miRNA-222-3p enhances the proliferation and suppresses the apoptosis of acute myeloid leukemia cells by targeting Axin2 and modulating the Wnt/b-catenin pathway

被引:2
|
作者
Liu, Zhenyan [1 ]
Zhong, Liang [2 ]
Dan, Wenran [1 ]
Chu, Xuan [1 ]
Liu, Chen [2 ]
Luo, Xu [1 ]
Zhang, Zhonghui [1 ]
Lu, Yang [1 ]
Wan, Peng [1 ]
Wang, Xiao [1 ]
Liu, Beizhong [1 ,2 ]
机构
[1] Chongqing Med Univ, Cent Lab Yongchuan Hosp, Chongqing 402160, Peoples R China
[2] Chongqing Med Univ, Dept Lab Med, Key Lab Lab Med Diagnost, Minist Educ, Chongqing 400016, Peoples R China
基金
中国国家自然科学基金;
关键词
MicroRNA-222-3p; Axin2; Wnt; b-catenin pathway; Acute myeloid leukemia; CANCER; MIGRATION; MICRORNAS; INVASION; PROMOTES;
D O I
10.1016/j.bbrc.2022.06.054
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
MicroRNA (miRNA)-222-3p is overexpressed in numerous tumors, where it acts as an oncogene. Although miRNA-222 is highly expressed in acute myeloid leukemia (AML), its functions and the mechanisms underlying these functions have not yet been fully elucidated. This study aimed to investigate the regulatory roles of miRNA-222-3p in AML and the molecular mechanisms underlying these roles. In this study, we observed that miRNA-222-3p increased the viability and suppressed the apoptosis of AML cells. Axin2 was demonstrated to be a direct target of miRNA-222-3p, which when overexpressed, inhibited Axin2 expression and stimulated the Wnt/b-catenin pathway. In contrast, upregulation of Axin2 expression levels reduced the viability and enhanced the apoptosis of AML cells. Moreover, it partially reversed the effects of the miRNA-222-3p mimic on the proliferation and apoptosis of, and modulation of the Wnt/b-catenin pathway in, AML cells. Taken together, this study provides strong evidence that miRNA-222-3p can serve as a molecular target for AML treatment. (c) 2022 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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页码:83 / 91
页数:9
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