MiR-29a expression is dependent on NPM-ALK. Using murine conditional models NPM-ALK fusion protein expression was analyzed by Western blotting (A) in lymph nodes of conditional NPM-ALK transgenic mice and (B) in MEF NPM-ALK cells in on and off conditions. β-actin was used as a loading control. In both models, miR-29a was detected by RT-qPCR in on and off conditions (histograms). Data are representative of 3 independent experiments. P for on vs off (*P < .05). (C) Human ALCL ALK⁺ cell lines (SU-DHL-1 and Karpas-299) were transiently transfected with an anti-ALK siRNA (siALK) or a control siRNA (Ctl) and inhibition of NPM-ALK protein expression was assessed by Western blotting. (D) ALCL cells were treated with an NPM-ALK inhibitor (PF-2341066) and its autophosphorylation status was detected with an antibody directed against phosphorylated-tyrosine 664 (NPM-ALK P-Y664). β-actin was used as a loading control. Expression levels of miR-29a, by RT-qPCR in ALCL cell lines after transfection with siALK (C) or treatment with PF-2341066 (D) are presented as the ratio of RQ (siALK/Ctl) and RQ (PF/Ctl) respectively. P for siALK vs Ctl and PF vs Ctl (*P < .05).