Table 2 The effects of statins on the apoptosis and senescence in different cancer cell lines
From: Paradoxical effects of statins on endothelial and cancer cells: the impact of concentrations
Statin | IC50 values | Cell line | Mechanism of effect | Effect on apoptosis |
|---|---|---|---|---|
Fluvastatin | 10 μM | MCF10A | The anticancer effect of statins is independent of prenylation of RAS family proteins and is associated with a cancer cell EMT phenotype [126] Inhibition of the RAS prenylation was uncoupled from fluvastatin-induced-apoptosis [126] | Induction of apoptosis |
Simvastatin Atorvastatin | Atorvastatin 0.3–49.1 µM, Simvastatin 0.2- 40.8 µM | Triple-negative breast cancer (TNBC) | MVA rescued the effects of these statins [127] | Induction of apoptosis |
Simvastatin | 12 and 8 μM | 12 and 8 μM in PC3 and LNCaP cell lines respectively | Induces subG1/G1 arrest [128] | Induction of apoptosis |
|  | 4.06 µM | breast cancer cell lines BoM-1833 (BoM) derived from MDA-231, MCF7/BoM, and T47D | Growth inhibition [129] | Induction of apoptosis |
Simvastatin | 0.481 µM | Adrenal carcinoma SW13 vimentin-positive (SW13-vim+) | Simvastatin targeting of vimentin may promote apoptotic cell death [130] | Induction of apoptosis |
Simvastatin | 60 µM | T47D breast cancer cell | Decreased the cyclin D1 expression and cell growth [131] | Induction of apoptosis |
Atorvastatin | 1.16 μM to 4.3 μM | MDA-MB-231 cells | Atorvastatin sensitivity correlates with decreased cholesterol levels in atorvastatin-treated cell [132] |  |
Simvastatin, fluvastatin |  | PC9 and PC9 GR4 (simvastatin:4 µM, fluvastatin: 2 µM) H460, H358, and PC9 BrM3 (simvastatin:12 µM, fluvastatin: 4 µM) | Decreases metastatic lung cancer cell survival in vitro synergistically with ABL tyrosine kinases inhibitor. Isoprenoid and mevalonate rescued the effects of statin [133] | Induction of apoptosis |
Fluvastatin | 5.3 µM | human A549 lung adenocarcinoma cells | PI3K inhibition [134] | Induction of apoptosis |
Lovastatin | Â | Anaplastic thyroid cancer cells | Blocking the membrane localization of RhoA and Rac. Mevalonate, GGPP rescued the effects of these statin [135] | Induction of apoptosis |
Lipophilic statins | Â | Osteosarcoma cells | Blocking RhoA-p42/p44 MAPKs-Bcl-2 survival pathway. RhoA agonist rescued the effects of statins [122] | Induction of apoptosis |
Lovastatin | 0.3 µM | Human prostate cancer cells | Induce senescence and cause G1 cell cycle arrest. GGPP/mevalonate, but not FPP were able to rescue the effects of statin [124] | Induction of apoptosis |
Pitavastatin | 10 μM | Breast cancer and melanoma tumors | Enhance effects of radiation on cellular senescence of radiation. 5 mM mevalonate rescued the effects of Pitavastatin [30] | Induction of apoptosis |
Simvastatin | 0.1 µM | Primary prostatic Normal epithelial cell lines RWPE-1 and PWR-1E | Exert cytostatic and senescent effects and partially induced apoptosis [125] | Induction of apoptosis |
Simvastatin | 10 μM | Primary prostatic normal epithelial cell lines RWPE-1 and PWR-1E cancer cells | In contrast, simvastatin had a cytotoxic effect both on normal and cancer cells. Combination of LDL-C and mevalonate rescued the effects of statin [125] | Induction of apoptosis |
Lovastatin | 0.3 µM | Prostate cancer cells: PC-3, DU-145, LNCaP | Senescence and G1 cell cycle arrest. GGPP, mevalonate, constitutively active RhoA (caRhoA) rescued the effects of lovastatin [124] | Induction of apoptosis |