Fig. 2

The mesenchymal subtype of PDAC is highly susceptible to the PP2A inhibitor phendione. a Morphology of PDAC cells after treatment with 1–2 µM phendione for 48 h; scale bars represent 100 µm; n = 3. b Mesenchymal PDAC cells were incubated with concentrations of phendione from 1 to 10 µM for 48 h. Flow cytometry using annexin-V/PI staining was carried out to detect cell vitality versus apoptosis; data are shown as mean values ± SD; n = 3. c Epithelial PDAC cells were treated with 1–10 µM phendione for 48 h and apoptosis was determined by flow cytometry for annexin-V/PI; n = 3. Data were statistically analyzed using two-way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). d, e Mesenchymal and epithelial PDAC cells were incubated with 10 µM phendione for up to 24 h. Annexin-positive cells were detected by flow cytometry; n = 2. Data were statistically analyzed using unpaired t-test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). f Mesenchymal and epithelial murine PDAC cell lines were treated with 3 µM phendione for 24 h. PR130 was measured by immunoblot. HSP90 served as loading control; n = 2. g PDAC cells were cultured with 3 µM phendione for 1 h, 3 h, and 6 h. Phosphorylated forms of KAP1 (S824), AKT (S473), and ERK (T202/Y204), as well as total PR130 and p53 were detected by immunoblot. HSP90 and β-actin served as independent loading controls; n = 3