Fig. 4

β-peltatin inhibits the growth of PAC cells by inducing G2/M cell cycle arrest and mitochondrial apoptosis. Cell viability of PAC cells (A, B) was examined following treatment with the indicated concentrations of β-peltatin for 24 h, 48 h and 72 h. Representative images of cell cycle distribution of PAC cells (C, D) following administration of 0–4 nM β-peltatin for 12–48 h, respectively. Quantification data of cell cycle distribution of PAC cells (E, F). The expression of G2/M phase-related proteins in PAC cells (G, H) were examined using immunoblotting following treatment with β-peltatin at concentrations of 0, 1, 2 and 4 nM for 12 h. The expression levels were normalized to GAPDH. Following 48 h of β-peltatin administration, the apoptotic PAC cells were assessed by Annexin V-FITC and PI-stained flow cytometry (I, J) and quantified (right panel). The expression levels of apoptosis-related proteins were evaluated by immunoblotting in MIA PaCa-2 (K, L) and BxPC-3 (M, N) cells with β-peltatin treatment at the indicated intervals and doses. The expression levels were normalized to β-actin. 0.5 μM of GEM was chosen as the positive control. Results are presented as mean ± S.D. of triplicate independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, compared with the control