OBJECTIVES Currently, lncRNA plays an important role in the occurrence and development of acute myeloid leukemia (AML), including SNHG5. However, the role and mechanism of SNHG5 in AML remains unclear. In this study, we explored the regulatory mechanism of SNHG5 in the development of AML. METHODS AND RESULTS QRT-PCR was used to investigate the expression of SNHG5, miR-489-3p, and SOX. The proliferation and apoptosis of AML cells were analyzed by cell transfection, cell counting kit-8 (CCK8), and flow cytometric analysis. Moreover, the expression analysis of marker proteins was detected by western blot. Through luciferase activity assay, RNA pull-down, and RNA-binding protein immunoprecipitation (RIP), we proved that SNHG5 could bind miR-489-3p and SOX4 which might be the target gene of miR-489-3p. RESULTS We first found that SNHG5 was up-regulated in both AML patient bone marrow samples and various AML cell lines. Second, we found that knockdown of SNHG5 inhibited proliferation of AML cells and promoted apoptosis. It was found that SNHG5 could bind miR-489-3p, and the relative expression of SNHG5 was negatively correlated with miR-489-3p. Further results suggested that SOX4 might be the target gene of miR-489-3p. Finally, our experimental data indicated that knockdown of SNHG5 could reduce the tumor volume and down-regulated SOX4 levels in vivo. CONCLUSIONS Our results demonstrated that SNHG5 affected the expression of SOX4 through binding miR-489-3p to regulate proliferation and apoptosis of AML, which might act as a prospective prognostic biological marker and a promising therapeutic target for AML.

中文翻译：

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LncRNA SNHG5通过竞争性结合miR-489-3p在急性髓细胞白血病中调节SOX4的表达。

目的目前，lncRNA在包括SNHG5在内的急性髓细胞白血病（AML）的发生和发展中起着重要作用。但是，尚不清楚SNHG5在AML中的作用和机制。在这项研究中，我们探讨了SNHG5在AML发展中的调控机制。方法与结果QRT-PCR检测SNHG5，miR-489-3p和SOX的表达。通过细胞转染，细胞计数试剂盒8（CCK8）和流式细胞术分析了AML细胞的增殖和凋亡。此外，通过蛋白质印迹法检测标记蛋白的表达分析。通过荧光素酶活性测定，RNA下拉和RNA结合蛋白免疫沉淀（RIP），我们证明SNHG5可以结合miR-489-3p和SOX4，这可能是miR-489-3p的靶基因。结果我们首先发现SNHG5在AML患者的骨髓样本和各种AML细胞系中均被上调。其次，我们发现SNHG5的抑制可抑制AML细胞的增殖并促进细胞凋亡。发现SNHG5可以结合miR-489-3p，并且SNHG5的相对表达与miR-489-3p负相关。进一步的结果表明，SOX4可能是miR-489-3p的靶基因。最后，我们的实验数据表明，敲除SNHG5可以减少体内的肿瘤体积和下调SOX4水平。结论我们的结果表明SNHG5通过与miR-489-3p结合以调节AML的增殖和凋亡而影响SOX4的表达，这可能作为AML的预后生物学指标和有希望的治疗靶标。