Acute myeloid leukemia (AML) is a highly heterogeneous disease that remains untreatable. MicroRNAs (miRNAs or miRs) play important roles in the pathogenesis of leukemia. miR-21 is highly expressed in multiple types of human cancer and displays oncogenic activities; however, the clinical significance of miR-21 in AML remains unclear. In the present study, it was demonstrated that miR-21 levels were high in patients with AML and in AML cell lines. Further experiments demonstrated that overexpression of miR-21 in Thp-1 human monocytes derived from acute mononuclear leukemia peripheral blood promoted cell proliferation, while downregulation of miR-21-5p, a mature sequence derived from the 5' end of the miR-21 stem-loop precursor (another mature sequence, miR-21-3p, is derived form 3' end of miR-21), inhibited cell proliferation. Specifically, it was observed that overexpression of miR-21 could promote the transition of Thp-1 cells into the S and G2/M phases of the cell cycle, as shown by flow cytometry. Furthermore, inhibition of miR-21-5p arrested cells in the S and G2/M phases. Finally, BCL11B was determined to be a functional target of miR-21-5p by luciferase assays. Our study revealed functional and mechanistic associations between miR-21 and BCL11B in Thp-1 cells, which could serve to guide clinical treatment of AML.
Keywords: BCL11B; Thp-1 monocytes; acute myeloid leukemia; miR-21-5p.
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