LXR activation inhibits BPDCN cell proliferation. (A) Left panel, eFluor-labeled CAL-1 cells were treated with increasing noncytotoxic concentrations (1 µM, 5 µM, and 10 µM) of LXR agonists, T0901317 (T09) or GW3965 (GW), for 72 hours. Cell proliferation was assessed by eFluor dilution analyzed by flow cytometry. Histograms show 1 representative experiment of 10. Right panel, Cumulative data from the 10 independent experiments are expressed as relative proliferation (mean ± SEM) with the vehicle condition being considered as 100%. Data depicted for LXR agonist treatment illustrate the highest concentration, 10 µM T0901317 (T09) or GW3965 (GW) (***P < .001, Wilcoxon). (B) Left panel, CAL-1 cells were treated with 10 µM T09, GW, or vehicle control for 24, 48, or 72 hours. Cell cycle phase distribution was assessed by cytometry (n = 5). Right panel, Cumulative data from 5 independent experiments are expressed as percentage of cells in each cell cycle phase (mean ± SEM) for the highest concentration of LXR agonists, 10 µM (*P < .05, **P < .01,***P < .001, Wilcoxon). PI, propidium iodide.