HMG-CoA Reductase

Statin-Related Inhibition of Dehydroepiandrosterone Sulfate (DHEAS) Uptake by SLCO2B1 in Prostate Cancer (PC) Cells. B, Uptake of DHEAS in PC cells with 2.5 µM DHEAS and different concentrations of statins when incubated for 60 minutes. Statistical analysis was performed by comparing each condition with the DHEAS 2.5 µM and no statin state except when indicated. C, Uptake of DHEAS in PC cells before (scrambled short hairpin RNA) and after (short hairpin RNA 2B1) SLCO2B1 is knocked down when incubated with 2.5 μM DHEAS and 100 μM atorvastatin for 10 and 60 minutes. Statistical analysis was performed by comparing each condition with scrambled short hairpin RNA after 10 minutes with DHEAS except when indicated. P = .02 for the comparison between scrambled short hairpin RNA with 10 vs 60 minutes of DHEAS incubation for LNCaP and .01 for 22RV1. Other P values are indicated in the figure. Bars indicate means and error bars indicate standard deviation.

MDA-MB-231 cells were treated with simvastatin (SIM) or rosuvastatin (ROSU) in combination with ZOL for 48 h. Vitality and apoptosis were measured by using the cell titer blue and the caspase 3/7 Glo assay. Data are shown as mean ± SD of at least three individual experiments (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).

Western blotting showed that in U87 cells treated with pitavastatin, the LC3-II isoform dramatically increased after statin treatment and showed at day 2, 3 and 4.

To evaluate the role of cell cycle progression in androgen induced DSB formation, LAPC4 cells were either treated with solvent control or 50 μM lovastatin for 36 h prior to stimulation with 100 nM DHT for 6 h. Note that androgen induced γH2A.X foci formation was not different between control and lovastatin pre-treated cells.

The concentration of lanosterol slightly increases (f) and that of desmosterol significantly increases (g) in the brains of fluvastatin-treated 129.Mecp2tm1.1Bird/Y mice at P70 (n = 4 mice per group; P = 0.042). *P ≤ 0.05 determined using Dunnett’s post-hoc test to compare statin- with vehicle-treated groups. All error bars represent the s.e.m.

Micrographs of hematoxylin and eosin-stained liver sections from untreated and atorvastatin-treated TO mouse. Results of representative experiment of liver specimens incubated in vitro at 37癈 with and without 1.0 礛 atorvastatin for 6 hr is shown. A liver specimen at 0 hr is also shown. Liver structure and cytology are preserved in treated and untreated specimens. Inflammation and cholestasis are absent. (Hematoxylin and eosin, 10?and 40?.

B, Uptake of DHEAS in PC cells with 2.5 µM DHEAS and different concentrations of statins when incubated for 60 minutes. Statistical analysis was performed by comparing each condition with the DHEAS 2.5 µM and no statin state except when indicated.

Sterol-starved HepG2 cells were treated with vehicle or mevastatin for 24 h before exposure to the indicated concentrations of MK-2206 for a further 14 h. Cells were then harvested and subjected to Western blot analysis. Upper panel shows one representative blot from six experiments. Lower panel: the immunoblots data were plotted relative to vehicle-treated cells. Error bars represent SD. One, two and three asterisks indicate p < 0.05, p < 0.01 and p < 0.001, respectively, compared with matched vehicle-treated cells.

Statin-Related Inhibition of Dehydroepiandrosterone Sulfate (DHEAS) Uptake by SLCO2B1 in Prostate Cancer (PC) Cells. B, Uptake of DHEAS in PC cells with 2.5 µM DHEAS and different concentrations of statins when incubated for 60 minutes. Statistical analysis was performed by comparing each condition with the DHEAS 2.5 µM and no statin state except when indicated. C, Uptake of DHEAS in PC cells before (scrambled short hairpin RNA) and after (short hairpin RNA 2B1) SLCO2B1 is knocked down when incubated with 2.5 μM DHEAS and 100 μM atorvastatin for 10 and 60 minutes. Statistical analysis was performed by comparing each condition with scrambled short hairpin RNA after 10 minutes with DHEAS except when indicated. P = .02 for the comparison between scrambled short hairpin RNA with 10 vs 60 minutes of DHEAS incubation for LNCaP and .01 for 22RV1. Other P values are indicated in the figure. Bars indicate means and error bars indicate standard deviation.

MDA-MB-231 cells were treated with simvastatin (SIM) or rosuvastatin (ROSU) in combination with ZOL for 48 h. Vitality and apoptosis were measured by using the cell titer blue and the caspase 3/7 Glo assay. Data are shown as mean ± SD of at least three individual experiments (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).

Western blotting showed that in U87 cells treated with pitavastatin, the LC3-II isoform dramatically increased after statin treatment and showed at day 2, 3 and 4.

To evaluate the role of cell cycle progression in androgen induced DSB formation, LAPC4 cells were either treated with solvent control or 50 μM lovastatin for 36 h prior to stimulation with 100 nM DHT for 6 h. Note that androgen induced γH2A.X foci formation was not different between control and lovastatin pre-treated cells.

The concentration of lanosterol slightly increases (f) and that of desmosterol significantly increases (g) in the brains of fluvastatin-treated 129.Mecp2tm1.1Bird/Y mice at P70 (n = 4 mice per group; P = 0.042). *P ≤ 0.05 determined using Dunnett’s post-hoc test to compare statin- with vehicle-treated groups. All error bars represent the s.e.m.

Micrographs of hematoxylin and eosin-stained liver sections from untreated and atorvastatin-treated TO mouse. Results of representative experiment of liver specimens incubated in vitro at 37癈 with and without 1.0 礛 atorvastatin for 6 hr is shown. A liver specimen at 0 hr is also shown. Liver structure and cytology are preserved in treated and untreated specimens. Inflammation and cholestasis are absent. (Hematoxylin and eosin, 10?and 40?.

B, Uptake of DHEAS in PC cells with 2.5 µM DHEAS and different concentrations of statins when incubated for 60 minutes. Statistical analysis was performed by comparing each condition with the DHEAS 2.5 µM and no statin state except when indicated.

Sterol-starved HepG2 cells were treated with vehicle or mevastatin for 24 h before exposure to the indicated concentrations of MK-2206 for a further 14 h. Cells were then harvested and subjected to Western blot analysis. Upper panel shows one representative blot from six experiments. Lower panel: the immunoblots data were plotted relative to vehicle-treated cells. Error bars represent SD. One, two and three asterisks indicate p < 0.05, p < 0.01 and p < 0.001, respectively, compared with matched vehicle-treated cells.