Bcl-2 degradation is an additional pro-apoptotic effect of polo-like kinase inhibition in cholangiocarcinoma cells

Figure 1 PLK-inhibitor BI6727 reduces cell viability and acts pro apoptotic in cholangiocellular carcinoma cell lines. Cell viability of CCA cell lines KMCH-1 (A) and Mz-Ch-1 (D) treated with the PLK-inhibitor BI6727 (200 nmol/L for 24 h), the cytostatic drug cisplatin (1 mmol/L for 24 h) or both components was assessed by MTT assay (A, D) shown as % of viable cells (viability) compared to vehicle-treated cells (mean ± SEM, n = 3). Apoptotic nuclei were determined in DAPI stained KMCH (B) and Mz-Ch-1 (E) cells after treatment using fluorescence microscopy. The number of apoptotic nuclei was normalized to the total number of nuclei (mean ± SEM, n = 4). Apoptosis induction in KMCH-1 (C) and Mz-Ch-1 (F) cells was measured by fluorescent Caspase-3/-7 activity assay shown as foldchange of vehicle-treated cells (mean ± SEM, n = 3). PLK: Polo-like kinase; CCA: Cholangiocarcinoma; MTT: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid; DAPI: 4’, 6-diamino-2-phenylindole dihydrochloride.