MicroRNAs (miRNAs) function as post-transcriptional gene expression regulators. Some miRNAs, including the recently discovered miR-582–3p, have been implicated in leukemogenesis. This study aimed to reveal the biological function of miR-582–3p in acute myeloid leukemia (AML), which is one of the most frequently diagnosed hematological malignancies. The expression of miR-582–3p was determined using quantitative real-time PCR in blood samples from leukemia patients and in cell lines. Cell proliferation and cell cycle distribution were analyzed using the CCK-8, colony formation and flow cytometry assays. The target gene of miR-582–3p was verified using a dual-luciferase reporter assay. The G2/M phase arrest-related molecule contents were measured using western blotting analysis. We found miR-582–3p was significantly downregulated in the blood samples from leukemia patients and in the cell lines. MiR-582–3p overexpression significantly impaired cell proliferation and induced G2/M cell cycle arrest in THP-1 cells. Furthermore, cyclin B2 (CCNB2) was confirmed as a target gene of miR-582–3p and found to be negatively regulated by miR-582–3p overexpression. More importantly, CCNB2 knockdown showed suppressive effects on cell proliferation and cell cycle progression similar to those caused by miR-582–3p overexpression. The inhibitory effects of miR-582–3p overexpression on cell proliferation and cell cycle progression were abrogated by CCNB2 transfection. These findings indicate new functions and mechanisms for miR-582–3p in AML development. Further study could clarify if miR-582–3p and CCNB2 are potential therapeutic targets for the treatment of AML.

中文翻译：

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MicroRNA-582-3p 通过靶向细胞周期蛋白 B2 负调控急性髓性白血病的细胞增殖和细胞周期进程。

MicroRNAs (miRNAs) 作为转录后基因表达调节剂发挥作用。一些 miRNA，包括最近发现的 miR-582-3p，与白血病发生有关。本研究旨在揭示 miR-582-3p 在急性髓细胞白血病 (AML) 中的生物学功能，AML 是最常被诊断出的血液系统恶性肿瘤之一。使用来自白血病患者的血液样本和细胞系中的定量实时 PCR 测定 miR-582-3p 的表达。使用CCK-8、集落形成和流式细胞术分析细胞增殖和细胞周期分布。使用双荧光素酶报告基因测定验证了 miR-582-3p 的靶基因。使用蛋白质印迹分析测量 G2/M 期阻滞相关分子含量。我们发现 miR-582-3p 在白血病患者的血液样本和细胞系中显着下调。MiR-582-3p 过表达显着损害细胞增殖并诱导 THP-1 细胞中的 G2/M 细胞周期停滞。此外，细胞周期蛋白 B2 (CCNB2) 被证实为 miR-582-3p 的靶基因，并发现其受到 miR-582-3p 过表达的负调控。更重要的是，CCNB2 敲低对细胞增殖和细胞周期进程的抑制作用类似于由 miR-582-3p 过表达引起的抑制作用。CCNB2转染消除了miR-582-3p过表达对细胞增殖和细胞周期进程的抑制作用。这些发现表明 miR-582-3p 在 AML 发展中的新功能和机制。