Abstract: Objective MicroRNAs (miRNAs, miRs) have emerged as critical regulators of tumor cell proliferation. This paper is to investigate how miR-221 is involved in the process of chronic myeloid leukemia (CML) and its working mechanisms.Methods Quantificational real-time polymerase chain reaction,qRT (qRT-PCR) was used to measure the expression of miR-221 in CML patients and control patients. K562 cells were transfected with miR-221 mimics, inhibitors, or negative controls. MTT assay was used to determine cell viability. Flow cytometry was used to measure the cell apoptosis and cell cycle. Bioinformatics was used to predict the target gene of miR-221, the qRT-PCR and Western blot were used to determine the expression of p27^Kip1 expression. Results The expression of miR-221 was increased significantly in the bone marrow cells in CML patients compared with control patients. Overexpression the miR-221 significantly increased cell vitality and promoted cell proliferation and G1-to-S phase transition of the cell cycle in K562 cells, while inhibition of miR-221 rescued the results. p27^Kip1 is the important target gene regulated by miR-221, the inhibition of the miR-221 promoted the p27^Kip1 expression, while miR-221 overexpression decreased the p27^Kip1 expression. Conclusion Our study suggested that miR-221 may be an oncogenic miRNA by inhibiting the protein expression of p27^Kip1 in CML.

Key words: chronic myeloid leukemia, miR-221, K562 cells, p27^Kip1