Figure 1

Statin-induced apoptosis and its lipid dependency in NSCLC cells. (A) Evaluation of caspase 3 activation in cells treated with up to 100 µM of either pitavastatin or fluvastatin for 48 h. Mevalonic acid (Mev, 1 mM) was used as rescue control counteracting statin-mediated intracellular depletion of sterol precursors. Mev and statin co-treated cells showed caspase 3 activity indistinguishable from untreated cells. One-way ANOVA, α = 0.05; Calu6 (pitavastatin): F(9,22) = 4.805, p = 0.0013; Calu6 (fluvastatin): F(9,16) = 2.207, p = 0.0801; H1993 (pitavastatin): F(9,26) = 1.337, p = 0.2664; H1993 (fluvastatin): F(9,21) = 2.794, p = 0.0252; A549 (pitavastatin): F(9,30) = 4.152, p = 0.0015; A549 (fluvastatin): F(9,18) = 3.411, p = 0.0128. Data are given as arithmetic mean of fold change relative to untreated control (CTL) ± SD from three independent experiments. Asterisks denote statistical significance as determined via Dunnett’s multiple comparison test compared to untreated control (CTL): *p < 0.05; **p < 0.01; ***p < 0.001. (B) Morphological changes associated with statin exposure compared to untreated cells or mevalonate rescue control. (C) Assessment of PARP cleavage (cPARP) in cells treated with 100 µM pitavastatin (P) or fluvastatin (F) alone or in combination with 1 mM mevalonic acid (Mev) for 48 h via 10% SDS-PAGE and Western Blot. β-actin was used as loading control.