Abstract

BackgroundMicroRNAs (miRNAs) are a class of small non-coding RNAs that have been shown to play a crucial role in normal hematopoiesis and leukemogenesis. Differentiation arrest is the hallmark of acute myeloid leukemia (AML). However, key miRNAs regulating differentiation arrest in AML remain unclear. MethodsSmall RNA-seq was performed in paired bone marrow samples at initial diagnosis vs. complete remission (CR) and differentially expressed miRNAs (DEMs) were analyzed for each patient. The mRNA levels of significantly upregulated miRNAs in all the patients were assayed during myeloid differentiation induced by all-trans retinoic acid (ATRA) in HL-60 and NB4 cells by Q-PCR. HL-60 and NB4 cells were infected with miR-3913-5p lentivirus (Lenti-miR-3913-5p), and the myeloid differentiation rate was assessed by flow cytometry as well as May–Grünwald Giemsa staining. CCK-8 assay was performed to detect the proliferation of cells. ResultsmiR-3913-5p and other 17 miRNAs were significantly upregulated at initial diagnosis vs. complete remission, and decreased in ATRA-induced myeloid differentiation of HL-60 cells and NB4 cells. Overexpression of miR-3913-5p inhibited myeloid differentiation, while had little effect on proliferation, in HL-60 and NB4 cells. ConclusionsmiR-3913-5p is a novel key regulator of cell differentiation arrest in AML.

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