miR-193a targets ETO, DNMT3a, HDAC3, KIT, CCND1, and MDM2 directly, and PTEN indirectly. (A) The sequences indicate the putative interaction sites between the miR-193a seed region (nucleotides 2-8) and the 3′ UTRs of ETO, DNMT3a, HDAC3, KIT, CCND1, and MDM2 WT or mutated derivatives. (B) pCDNA3.0 control plasmids and miR-193a–expressing plasmids were cotransfected with a modified luciferase pGL-3 control vector containing ETO, DNMT3a, HDAC3, KIT, CCND1, and MDM2 3′-UTRs or their mutants as indicated. Luciferase assays were performed 48 hours after transfection. Each histogram shows normalized mean values of relative luciferase activity from 3 independent experiments. Normalized luciferase activity in the absence of miR-193a expression vector was set to 100%. (C) The effectiveness of synthetic miR-193a on ETO, DNMT3a, HDAC3, AML1/ETO, KIT, CCND1, and MDM2 proteins was analyzed by Western blot. (D) AML1/ETO⁺ had higher KIT levels (P = .0004). (E) miR-193a increases PTEN expression indirectly. SKNO-1 cells (mock, and si-A/E) were transfected with synthetic miR-193a or scramble oligonucleotides for 48 hours. Relative PTEN levels were evaluated by qRT-PCR. The results represent the average of 3 independent evaluations ± SD.