Fig. 1.

Anticancer activity of simvastatin and romidepsin in bladder cancer cells. (A) Cells were treated for 48 h with 2.5–40 μM simvastatin and cell viability was measured using CCK-8 assay. Mean ± SD, n = 6. (B) Cells were given 2.5–10 μM simvastatin and confluence measurements were performed at 3-hour intervals over 3 days. Mean ± SD, n = 6. (C) Western blotting for AMP-activated protein kinase (AMPK), acetylated histone, glucose-regulated protein (GRP) 78, endoplasmic reticulum resident protein (ERp) 44, and peroxisome proliferator-activated receptor (PPAR) γ. Cells were treated for 48 h with 2.5–20 μM simvastatin. Actin was used for the loading control. Representative blots are shown. (D) Cells were treated for 48 h with different concentrations of various histone deacetylase (HDAC) inhibitors, and cell viability was measured using CCK-8 assay. Mean ± SD, n = 6. (E) Cells were treated for 48 h with 10–160 nM romidepsin and cell viability was measured using CCK-8 assay. Mean ± SD, n = 6. (F) Cells were given 10–40 nM romidepsin and confluence measurements were performed at 3-hour intervals over 3 days. Mean ± SD, n = 6. (G) Western blotting for acetylated histone, GRP78, and ERp44. Cells were treated for 48 h with 10–40 nM romidepsin. Actin was used for the loading control. Representative blots are shown.