Depletion of miR-126 increases sensitivity to chemotherapy treatment in mice carrying AE9a-induced AML. (A) AE9a, AE9a+miR-126, and miR-126KO+AE9a tertiary leukemic recipient mice were treated with phosphate-buffered saline (control; solid line), or a daily dose of 100 mg/kg Ara-C for 5 days along with a daily dose of 3 mg/kg doxorubicin during the first 3 days of Ara-C treatment (indicated by _D and dashed line; 5+3 regimen³⁶ ). Kaplan-Meier curves are shown. (B) Wright-Giemsa–stained PB and BM, and H&E-stained spleen and liver of the treated tertiary BMT recipient mice at the end point. Bars represents 25 μm for PB and BM; 100 μm for spleen and liver. (C) The relative viability of Kasumi-1 and primary leukemia cells of t(8;21) AML patients treated with serial dilutions of doxorubicin and Ara-C for 48 hours. (D) Lentivirus-mediated inhibition of miR-126 was detected by qRT-PCR. The data shown are the means of 3 biological replicates. **P < .01. Error bars represent standard deviation. IC50, half-maximum inhibitory concentration miRZip-Con, miRZip™ control lentivirus (System Biosciences); miRZip-126, miRZip™ anti-miR-126 lentivirus (System Biosciences, Mountain View, CA).