Fig. 6
PRLR induces a senescence-like phenotype that is associated with chemoresistance. A SA-β-galactosidase staining in PRLR wt-tranduced (orange) and parental control (grey) HL-60 and SKM-1. *p < 0.05 (unpaired t test, n = 4). B p21 mRNA expression in PRLR-tranduced (orange) and parental control (grey) HL-60 and SKM-1 cells analysed by qPCR. Bars represented 2ΔCt ± SEM of three independent experiments. ***p < 0.001 (unpaired t test). C SA-β-galactosidase staining in HL-60 (n = 4, green), SKM-1 (n = 4, blue), MonoMac-1 (MM, n = 6, grey) and U-937 (n = 3, purple) cells. *p < 0.05 (one-way ANOVA, Tukey’s multiple comparison test). D SA-β-galactosidase staining in CRISPR/Cas9-tranduced (orange) and parental control (grey) U-937 clones (n = 3, one-way ANOVA, Dunnett’s multiple comparison test). E PRLR wt-transduced (orange) and parental control (grey) HL-60 and SKM-1 cells were treated for 48 h with increasing cytarabine doses alone (AraC, black) or in combination with 20 nM elimusertib (red). Viability was analysed by flow cytometry and representative results were graphicated. EC50 value was calculated (left), as well as the fold change in the EC50 (1-(EC50 AraC/cotreatment EC50) (n = 4, right); ***p < 0.001 (unpaired t test). In all graphs, bars represent the mean ± SEM