The expression of miR-139-5p is downregulated in CML patients. (A) Relative expression levels of miR-139-5p in the BM were compared among samples from normal healthy donors and patients as described in the figure. Each individual dot represents 1 sample. (B) Relative miR-139-5p expression in the PB was compared among samples as described in the figure. (C) Quantitative RT-PCR analysis of miR-139-5p expression in Lin⁻c-Kit⁺ HSPCs purified from control or p210^BCR-ABL-expressing mice. Data represent the mean ± standard error of the mean (SEM) (N = 4). (D) Expression of miR-139-5p in CML (K562 and Kcl22) was measured after 24-hour treatment of BCR-ABL inhibitor, STI571 (imatinib), or vehicle (dimethyl sulfoxide [DMSO]). Data represent the mean ± SEM (N = 6 for K562 cells; N = 5 for Kcl22 cells). (E) Expression of miR-139-5p in K562 cells was measured after 24-hour treatment of signaling inhibitors (LY294002 for PI3K/acutely transforming retrovirus [Akt] pathway; SP600125 for JNK pathway; PD98509 for MEK/extracellular signal-regulated kinase pathway) described in the figure. Data represent the mean ± SEM (N = 4). AML-M1, AML type 1; AML-M2, AML type 2; AML-M4, AML type 4; CML-CP, BCR-ABL–positive CML–chronic phase; CMPD-CNL, BCR-ABL–negative CMPD–chronic neutrophilic leukemia; CMPD-ET, BCR-ABL–negative CMPD–essential thrombocythemia; CMPD-MF, BCR-ABL–negative CMPD–myelofibrosis; CMPD-PV, BCR-ABL–negative CMPD–polycythemia vera.