Abstract
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.