Department of Hematology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
College of Life Sciences, China Jiliang University, Hangzhou, China.
Bioengineered. 2021 Dec;12(1):4508-4519. doi: 10.1080/21655979.2021.1956400.
To study the regulation of miR-148a-3p on CDK6 and its mechanism in the progress of acute myeloid leukemia (AML), differential miRNAs were analyzed by bioinformatics, and the miR-148a-3p levels in AML cell lines were detected. Results showed that miR-148a-3p played a crucial role in AML, and the level was lower in AML cells, especially in J111 and KG-1a cells. In J111 and KG-1a cells, the up-regulation of miR-148a-3p mimics blocked the cell growth by arresting cell cycle at G2/M and enhancing cell apoptosis. Transwell and EMT markers detection indicated that miR-148a-3p reduced the cell migration and invasion. Afterward, through bioinformatics analysis, it showed that the CDK6 is one of the direct target genes of miR-148a-3p. DLR assay confirmed the target regulation. CDK6 overexpression reversed the effects of miR-148a-3p on AML cells. Collectively, miR-148a-3p inhibited the process of AML cells through disturbing the CDK-6 expression, implying that the trageting miR-148a-3p might be regarded as effective therapy of AML.
为了研究 miR-148a-3p 对急性髓系白血病（AML）进展中 CDK6 的调控及其机制，通过生物信息学分析差异 miRNA，并检测 AML 细胞系中 miR-148a-3p 的水平。结果表明，miR-148a-3p 在 AML 中发挥着关键作用，其水平在 AML 细胞中较低，尤其是在 J111 和 KG-1a 细胞中。在 J111 和 KG-1a 细胞中，上调 miR-148a-3p 模拟物通过将细胞周期阻滞在 G2/M 期并增强细胞凋亡来阻止细胞生长。Transwell 和 EMT 标志物检测表明，miR-148a-3p 降低了细胞迁移和侵袭能力。随后，通过生物信息学分析，表明 CDK6 是 miR-148a-3p 的直接靶基因之一。DLR 测定证实了靶基因的调控。CDK6 过表达逆转了 miR-148a-3p 对 AML 细胞的作用。综上所述，miR-148a-3p 通过干扰 CDK-6 表达抑制 AML 细胞的进程，提示靶向 miR-148a-3p 可能成为 AML 的有效治疗方法。
