Figure 6 from Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer

MPZL3 loss enhances cisplatin and olaparib resistance in OVCAR4 cells. A, Dose–response curves were derived from cell viability assays (FluoReporter dsDNA quantification) of OVCAR4 cells expressing scr control or MPZL3 shRNAs (n = 4, mean ± SEM). B, IC₅₀ values derived from dose–response curves in A [n = 4; one-way ANOVA P = 0.0011 (cisplatin), P = 0.0003 (olaparib), and P = 0.2793 (paclitaxel); Dunnett multiple comparison test P values shown]. C, Western blot of MPZL3 knockdown OVCAR4 cells that were injected subcutaneously into Nod/SCID gamma mice. D, Subcutaneous tumor growth of OVCAR4 cells expressing scr control (left) or shMPZL3#1 (right) under vehicle (saline) or cisplatin treatment (two tumors per mouse, n = 4–5 mice per group). The start of cisplatin treatment is indicated with an arrow. E, Tumor growth rates under treatments for both scr control and shMPZL3#1 groups. Growth rates were calculated by dividing the final tumor volumes by the average tumor volumes from three measurements: 3 days before treatment, on the day treatment began, and 4 days after treatment began (median tumor volume shown, n = 8–10, Mann–Whitney test). F, Final tumor volume images of OVCAR4 subcutaneous tumors from both saline- and cisplatin-treated groups. All mice were euthanized after receiving the same doses of treatment. G, Immunofluorescence images and quantification of γH2AX signals induced by cisplatin (left) or olaparib (right) in OVCAR4 cells following MPZL3 knockdown [scale bar, 20 μm; n = 4; one-way ANOVA P = 0.0100 (cisplatin) and P = 0.0514 (olaparib); Dunnett multiple comparison test P values shown]. H, Caspase 3/7 activity induced by cisplatin (left) or olaparib (right) in OVCAR4 cells following MPZL3 knockdown [n = 4; repeated measures one-way ANOVA P = 0.0034 (cisplatin) and P = 0.0263 (olaparib); Dunnett multiple comparison test P values shown].