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. Author manuscript; available in PMC: 2014 May 30.
Published in final edited form as: Cancer Cell. 2010 Apr 13;17(4):388–399. doi: 10.1016/j.ccr.2010.02.027

Figure 2. Inhibition of Hh signaling by itraconazole is not mediated by effects on cholesterol biosynthesis.

Figure 2

(A) Increasing serum concentrations attenuated the inhibitory activity of itraconazole but not KAAD-cyclopamine. (B) The attenuating effect of serum was abolished by lipid depletion (LD). (C) Shh-Light2 cells were pretreated with methyl-β-cyclodextrin (MβCD) 8 mM in DMEM for 45 minutes to remove sterols from the cell surface (Cooper et al., 2003). Lovastatin, an HMG-CoA reductase inhibitor, inhibited Hh pathway activity induced by ShhN. Cholesterol, in ethanol solution, reversed the pathway inhibition due to lovastatin (D, E) Lathosterol, desmosterol, and cholesterol failed to rescue Hh pathway inhibition by itraconazole under low (D) or lipid depleted (E) serum conditions. All signaling assays were performed with Shh-Light2 cells and data are mean of triplicates ± s.d.

See also Figure S2.