Abstract
Previous studies have showed that the interaction between microRNAs (miRNAs) and leukemia stem cells (LSCs) may be a cause of drug resistance of acute myeloid leukemia (AML). However, whether miR-126 participates in the pathogenesis of AML remains unclear. In our study, we first examined the expression of miR-126 in CD34+ or CD34- cells isolated from blood samples and LSC cell line: KG-1a-LSCs and MOLM13-LSCs by qRT-PCR analysis. Then miR-126 inhibitor and mimics were applied to evaluate the roles of miR-126 in cell proliferation of LSC cell lines using CCK-8 assay and Ki-67 staining. Moreover, flow cytometry analysis was used to assess the apoptosis of LSC cell lines treated with miR-126 inhibitor of mimics. In addition, we analyzed the relationship between miR-126 and DNA methyltransferase 1 (DNMT1) by bioinformatics analysis and dual-luciferase reporter assay. Western blot analysis was applied to examine the protein expression level of DNMT1 in miR-126 mimics treated LSC cells. Results showed that miR-126 expression was significantly higher in CD34+ cells and KG-1a-LSCs and MOLM13-LSCs. Knockdown of miR-126 in KG-1a-LSCs and MOLM13-LSCs inhibited cell proliferation, and promoted apoptosis. miR-126 could regulate DNA methyltransferase 1 (DNMT1) expression by directly binding to it. In conclusion, these findings suggested that miR-126 may promote cell proliferation of LSCs by targeting DNMT1.