Abstract: Objective To investigate the function and mechanism of miR-150 in human chronic myeloid leukemia cell line K562. Methods clinic CML patients and normal controls were collected. The peripheral blood mononuclear cells from above CML and controls were isolated. Quantitative RT-PCR analysis was used to determine the expression level of miR-150 and c-Myb mRNA; miR-150 mimic and negative control were transfected into K562 cells, respectively. CCK-8 analysis was performed to examine K562 cell proliferation. FACS analysis was used to detect cell cycle. Dual-luciferase assay and Western blot were used to detect the influence of miR-150 on target gene c-Myb. Results when compared to the normal control, the miR-150 level was down-regulated in CML patients, whereas c-Myb expression was up-regulated in CML. Overexpression of miR-150 inhibits K562 cell proliferation and cell cycle progression. miR-150 could reduce c-Myb expression in K562 cells. Conclusions miR-150 is down-regulated in CML, and it can reduce K562 cell growth by repressing the expression of oncogene c-Myb.

Key words: miRNA, c-Myb, K562, cell cycle