Fig. 5

The anti-melanoma action of DDA in vivo is LXRβ-dependent. a Mice engrafted with SKMEL-28 cells transfected with shCTRL or sh4LXRβ (10 per group) were treated with DDA (i.p. 20 mg/kg/day) or vehicle. Mean tumor volumes ± S.E.M. are shown, **P < 0.01, analysis of variance (ANOVA). Data are representative of three independent experiments. b At the end of treatments, tumors were analyzed for Nur77, NOR1, and LC3 protein expression by immunoblotting. All images and blots are representative of three independent experiments. c, d Mice engrafted with mouse B16F10 cells or human SKMEL-28 (10 per group) were treated with vehicle, DDA (i.p. 20 mg/kg/day), TO (i.p. 20 mg/kg/day), and DDA + TO (i.p. 20 mg/kg/day each). Mean tumor volumes ± S.E.M. are shown, **P < 0.01, analysis of variance (ANOVA). Quantification of Δ8-sterols and 5,6α-EC and 5,6β-EC in tumors were quantified by GC/MS. The results are reported as µg Δ8-sterols or ng 5,6-EC/g tumors. e Box plot of TCGA RNA-seq data from patients with melanoma showing that LXRβ is the predominant LXR isoform expressed. ***P < 0.001