Fig. 5: PLK1 inhibition leads to increased senescence of KMT2C/KD cells.

a Representative photos of control and KMT2C/KD1 and KD2 HTB9 and T24 cells with or without PLKi treatment at two different concentrations (Un = Untreated, 10 nM, 30 nM), stained with SA-β-Gal staining solution. Graph showing the percentages of SA-β-Gal positive cells in control and KMT2C/KD1 and KD2 HTB9 cells) that have been treated or not with PLKi. In bargraphs, one-way ANOVA was used and statistically significant pairwise comparison with respective vehicle is indicated with stars on top of each column. b Western blots showing p21 and p16 levels from control and KMT2C/KD1 and KD2 HTB9 cells that have been treated with PLKi at three different concentrations (Un = Untreated, 10 nm, 30 nm). Antibody against GAPDH was used as loading control. c Tumor growth obtained from xenografts of control (top) and KMT2C/KD1 (bottom) HTB9 cells treated with vehicle or volasertib (12.5 mg/kgr, twice a week). Number of mice used: n = 7 for Scr and n = 9 for KD1. Mann-Whitney U test was used in statistical analysis of pairwise comparisons. d Immunofluorescence with antibody against p21 on tumor sections from vehicle and volasertib treated xenografts mice that were generated by control and KMT2C/KD1 HTB9 cells. e Western blot analysis and quantitation of p21 protein levels on tumor lysates from vehicle and volasertib treated xenograft mice that were generated by control and KMT2C/KD1 HTB9 cells. Student’s t test was used for statistical analysis. f Immunocytochemistry using GL-13 (Sentragor) on tumor sections from vehicle and volasertib treated xenografts mice that were generated by control and KMT2C/KD1 HTB9 cells. For all statistical analyses, ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05, ns not significant.