Oncology Letters 2016-01-01

MicroRNA-181a enhances the chemotherapeutic sensitivity of chronic myeloid leukemia to imatinib.

Guangyu Wang, Ran Zhao, Xingsheng Zhao, XI Chen, Dong Wang, Yinji Jin, XI Liu, CI Zhao, Yuanyuan Zhu, Chengcheng Ren, Minghui Li, Xiaoming Jin, Fengmin Zhang, Zhaohua Zhong, Tianzhen Wang, Xiaobo Li

Index: Oncol. Lett. 10 , 2835-2841, (2016)

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Abstract

MicroRNA-181 (miR-181) has been recently demonstrated to participate in the differentiation and development of immune cells, including natural killer cells and B and T lymphocytes, and myeloid linages, including erythroid and megakaryocytic cells. The aberrant expression of miR-181, particularly low expression levels, has been observed in a number of leukemia types, including B-cell chronic lymphocytic leukemia and cytogenetically abnormal acute myeloid leukemia. However, the expression and function of miR-181 in chronic myeloid leukemia (CML) remains unknown. In the present study, the aberrant expression of miR-181a was analyzed in a patient with CML and in the CML K562 cell line. In addition, the function and potential mechanisms of miR-181a in K562 cells with regard to their chemotherapeutic sensitivity to imatinib were investigated. The expression levels of miR-181a were significantly reduced in the patient with CML and in the CML K562 cell line. Furthermore, the overexpression of miR-181a in the K562 cells enhanced the chemotherapeutic sensitivity of these cells to imatinib. The potential mechanism mediating these effects may be associated with the capacity of miR-181a to inhibit cell growth and/or to induce cells apoptosis and differentiation in K562 cells. The results of the present study suggested that miR-181a may be a target for the treatment of CML and a useful indicator of the therapeutic sensitivity of CML to imatinib.