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.
journal_name
Oncol Lettjournal_title
Oncology lettersauthors
Wang G,Zhao R,Zhao X,Chen XI,Wang D,Jin Y,Liu XI,Zhao CI,Zhu Y,Ren C,Li M,Jin X,Zhang F,Zhong Z,Wang T,Li Xdoi
10.3892/ol.2015.3663subject
Has Abstractpub_date
2015-11-01 00:00:00pages
2835-2841issue
5eissn
1792-1074issn
1792-1082pii
OL-0-0-3663journal_volume
10pub_type
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