Abstract: Objective To investigate the function and mechanism of RNA binding protein QKI5 in human acute myeloid leukemia (AML). Methods The clinically diagnosed acute leukemia patients were collected as the experimental groups. The expression level of QKI mRNA were detected by RT-qPCR in experimental groups and normal controls. Lentivirus expressing QKI5 was used to transduce into HL-60 cells. CCK-8 analysis was performed to detect the influence of QKI5 on HL-60 cell proliferation. PI staining and FACS assay were used to assess the effects of QKI5 on HL-60 cell cycle progression. RT-qPCR were performed to investigate the changes of miRNA. Results QKI5 mRNA was down-regulated in AML compared to the normal control（p<0.05）. Overexpression of QKI5 repressed HL-60 cell proliferation and cell cycle progression. QKI5 specifically regulated the miR-124 biogenesis. miR-124 inhibits HL-60 cell proliferation via targeting c-Myc expression. Conclusions The QKI5~miR-124~c-Myc regulatory axis has important roles in acute myeloid leukemogenesis.

Key words: RNA binding protein, QKI5, microRNA-124, c-Myc, acute myeloid leukemia