小RNA
髓系白血病
癌症研究
细胞生长
下调和上调
细胞凋亡
白血病
U937电池
髓样
转染
生物
免疫学
细胞培养
基因
遗传学
作者
W L-Wang,Wang Hr,Ji Wg,Guo Sl,Li Hx,Xu Xy
出处
期刊:PubMed
日期:2019-06-01
卷期号:23 (11): 4842-4849
被引量:9
标识
DOI:10.26355/eurrev_201906_18071
摘要
To examine the expression level of microRNA-485-5p (miRNA-485-5p) in acute myeloid leukemia (AML) and its biological function in regulating the proliferative ability of AML through targeting SALL4.Serum level of miRNA-485-5p in AML patients and healthy controls was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MiRNA-485-5p level in AML cell lines was detected by qRT-PCR as well. Proliferative and apoptotic changes in AML5 and U937 cells overexpressing miRNA-485-5p were assessed. Subsequently, the regulatory effect of miRNA-485-5p on SALL4 level was evaluated. Rescue experiments were conducted to uncover the role of miRNA-485-5p/SALL4 regulatory loop in regulating cellular behaviors of AML.Compared with healthy controls, serum level of miRNA-485-5p was lower in AML patients. MiRNA-485-5p was similarly downregulated in AML cell lines. Overexpression of miRNA-485-5p stimulated proliferation and alleviated apoptosis in AML. SALL4 level was downregulated by transfection of miRNA-485-5p mimics in AML5 and U937 cells. Overexpression of SALL4 could reverse the regulatory effect of miRNA-485-5p on proliferative and apoptotic abilities of AML.MiRNA-485-5p is downregulated in AML. Overexpression of miRNA-485-5p alleviates the malignant progression of AML through downregulating SALL4.
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