Laboratory Medicine, Jingmen No. 1 People's Hospital, China.
FEBS Open Bio. 2020 May;10(5):734-743. doi: 10.1002/2211-5463.12814. Epub 2020 Mar 26.
Acute myeloid leukemia (AML) is the second most common type of leukemia worldwide. It was previously reported that expression of the long noncoding RNA LOC285758 is positively associated with AML cell proliferation, but the underlying mechanisms have not previously been reported. Here, we report that LOC285758 expression is higher in clinical AML blood samples and cultured AML cells. miR-204-5p was confirmed to be a target gene of LOC285758 by bioinformatics analysis and luciferase assay. LOC285758 overexpression promoted AML cell viability and invasion abilities, which were effectively inhibited by miR-204-5p overexpression; moreover, miR-204-5p overexpression also regulated the expression of E-cadherin, N-cadherin and Twist1. The data also showed that increased LOC285758 expression could effectively suppress the earlier effects of miR-204-5p on AML cells. Our findings suggest that targeting of miR-204-5p by LOC285758 promotes the cell viability and invasion of AML cells, and thus LOC285758 may have potential as a therapeutic target for AML treatment.
急性髓细胞白血病（AML）是全球第二常见的白血病类型。先前有报道称，长链非编码 RNA LOC285758 的表达与 AML 细胞增殖呈正相关，但尚未报道其潜在机制。在这里，我们报告临床 AML 血液样本和培养的 AML 细胞中 LOC285758 的表达更高。通过生物信息学分析和荧光素酶报告基因实验证实，miR-204-5p 是 LOC285758 的靶基因。LOC285758 的过表达促进了 AML 细胞的活力和侵袭能力，而过表达 miR-204-5p 可有效抑制这些作用；此外，miR-204-5p 的过表达还调节了 E-钙黏蛋白、N-钙黏蛋白和 Twist1 的表达。数据还表明，LOC285758 表达的增加可有效抑制 miR-204-5p 对 AML 细胞的早期作用。我们的研究结果表明，LOC285758 通过靶向 miR-204-5p 促进 AML 细胞的活力和侵袭，因此 LOC285758 可能有作为 AML 治疗的治疗靶点的潜力。
