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. 2019 Mar 1;10(18):1716–1728. doi: 10.18632/oncotarget.26733

Figure 1. Statins impair the viability of GBM and other cancer cells largely through TGF-β inhibition.

Figure 1

(A) IC50 (μM) values of simvastatin for U251MG, U87MG, and T98G GBM cells with 1%FBS-MEM medium for 6 days. (B) IC50 (μM) values of simvastatin for GICs. (C) IC50s (μM) of simvastatin-treated lung cancer H1229, prostate cancer PC-3, breast cancer MDA-MB-231 and melanoma VMM39. Cell proliferation measured at OD570nm. (D) IC50 for simvastatin demonstrates a significant inverse correlation with normalized SBE4-luciferase activity in GBM lines (left panel), seven GIC lines (middle panel) and four other cancers (right panel). (E) SBE4 activity +/- exogenous TGF-β in seven GICs. (F) Simvastatin lowered SBE4-luciferase activity at physiologically relevant concentrations (IC50 0.04μM) in high-TGF-β activity U251. (G) Simvastatin lowered SBE4-luciferase activity in six GIC lines. (H) Simvastatin inhibited SBE4-luciferase activity in a dose-dependent fashion in melanoma, breast, prostate, and lung cancer lines. (I) Simvastatin, lovastatin, and mevastatin reduced SBE4-luciferase activity in two high TGF-β activity GIC lines JWL-022 and G34, and exogenous TGF-β sensitized the effect. (J) Simvastatin reduced expression of the TGF-β target proteins ZYX and SERPINE1 in U251MG and G34 cells. Sim: simvastatin. Lova: lovastatin. Meva: mevastatin. All values are the mean±SD of three experiments. *, P<0.05; **, P<0.01. ***, P<0.001. ****, P<0.0001.