Skip to main content
. 2022 Aug 25;41(39):4459–4473. doi: 10.1038/s41388-022-02429-0

Fig. 4. PLK1 inhibition induces a sustained change in cell fate.

Fig. 4

A Schematic of the drug wash-out experiment. SUM149PT cells were treated for 3 days with rigosertib or DMSO. Subsequently, the drug was washed out and cells were cultured for eight more days without the drug and then harvested for downstream experiments. B Immunoblot showing levels of ERα and ERK2 (loading control) in SUM149PT cells treated with the indicated concentrations of rigosertib as depicted in Fig. 4A. C Bar graphs representing average mRNA expression of ESR1 and downstream targets in SUM149PT cells treated with 100 nM rigosertib or DMSO as depicted in Fig. 4A. n = 2 experimental replicates with 2 technical replicates each. Unpaired Student’s t-test. Data are means ± SD. D Representative flow-cytometry dot plots of EdU/Hoechst cell cycle staining of SUM149PT cells treated with 100 nM rigosertib or DMSO as depicted in Fig. 4A. E Bar graph depicting the proportion of cells in different cell cycle states based on EdU/Hoechst cell cycle staining shown in Fig. 4D. n = 3 experimental replicates. Ordinary two-way ANOVA with multiple comparisons. Data are means ± SD. F Schematic of the experimental setup for in vitro treated SUM149PT cells grown as mouse xenografts in NSG mice. Cells were treated for 3 days with 1 µM rigosertib or DMSO prior to injection. G Kinetics of primary tumour growth of SUM149PT cells treated in vitro with 1 µM rigosertib (n = 5 mice) or DMSO (n = 5 mice) as depicted in Fig. 4F. Mann–Whitney U-test. Data are means ± SD. H Left panel: Pie charts depicting quantification of tumour incidence upon in vitro treatment of SUM149PT cells as in Fig. 4F. Right panel: Table summarizing the frequency of tumour initiating cells (TICs) and respective statistical analysis. Chi-square test.