RESEARCH ARTICLE Radotinib Induces Apoptosis of CD11b+ Cells Differentiated from Acute Myeloid Leukemia Cells Sook-Kyoung Heo1, Eui-Kyu Noh2, Dong-Joon Yoon1, Jae-Cheol Jo2, Yunsuk Choi2, SuJin Koh2, Jin Ho Baek2, Jae-Hoo Park3, Young Joo Min2, Hawk Kim1,2* 1 Biomedical Research Center, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, 682-060, Republic of Korea, 2 Department of Hematology and Oncology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, 682-714, Republic of Korea, 3 Department of Hematology and Oncology, Myongji Hospital, Gyeonggi-do, 412-270, Republic of Korea *
[email protected] Abstract Radotinib, developed as a BCR/ABL tyrosine kinase inhibitor (TKI), is approved for the sec- OPEN ACCESS ond-line treatment of chronic myeloid leukemia (CML) in South Korea. However, therapeutic Citation: Heo S-K, Noh E-K, Yoon D-J, Jo J-C, Choi effects of radotinib in acute myeloid leukemia (AML) are unknown. In the present study, we Y, Koh S, et al. (2015) Radotinib Induces Apoptosis of demonstrate that radotinib significantly decreases the viability of AML cells in a dose-de- CD11b+ Cells Differentiated from Acute Myeloid Leukemia Cells. PLoS ONE 10(6): e0129853. pendent manner. Kasumi-1 cells were more sensitive to radotinib than NB4, HL60, or THP- doi:10.1371/journal.pone.0129853 1 cell lines. Furthermore, radotinib induced CD11b expression in NB4, THP-1, and Kasumi- Academic Editor: Rajasingh Johnson, University of 1 cells either in presence or absence of all trans-retinoic acid (ATRA). We found that radoti- Kansas Medical Center, UNITED STATES nib promoted differentiation and induced CD11b expression in AML cells by downregulating Received: March 30, 2015 LYN.