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. Author manuscript; available in PMC: 2022 Jun 30.
Published in final edited form as: Leukemia. 2020 Nov 12;35(7):1976–1989. doi: 10.1038/s41375-020-01088-y

Figure 2: NIK-positive ALK− ALCL lines are more dependent on activated NIK-IKKα signaling.

Figure 2:

A. left: Indicated ALCL lines were transduced with IKKα or Ctrl sgRNAs along with GFP. The fraction of viable sgRNA-expressing cells relative to the total viable cell fraction at indicated times following induction of the indicated sgRNAs, normalized to day 0 values. Error bars denote SD of triplicates. right: Indicated ALCL lines were transduced with IKKα or Ctrl sgRNAs, selected and expression induced. Lysates were analyzed by immunoblotting for the indicated proteins. B. left: Same as (A). Error bars denote SD of triplicates. right: Same as (A). Lysates were analyzed by immunoblotting for the indicated proteins. C. left: Indicated lines were treated with NIK inhibitor at the indicated concentrations for 4 days. Viability was measured by the MTS assay and normalized to DMSO-treated cells. Error bars denote SEM of triplicates. P were calculated comparing DMSO and treated groups; * indicates P < 0.05; ** indicates P < 0.01. right: ALK+ DEL and ALK− TLBR2 lines were treated with NIK inhibitor at the indicated concentrations overnight. Lysates were analyzed by immunoblotting for the indicated proteins. The relative p100 and p52 signal intensity (compared to β-actin) were determined by densitometric analysis, and normalized to untreated conditions in DEL line (right). Error bars denote SEM of three independent experiments.