Fig. 7: Expression of sPIRp21 does not potentiate the mechanism of cell killing by UV, CDDP and Chk1 inhibition in non-cancerous HFL1 cells.
A Representative images of HFL1 (left panel) and U2OS (right panel) cells transduced with the indicated vectors. Detection of p21 variants was performed by immunofluorescence using a specific myc-tag antibody. B Percentage (mean ± SD) of cells expressing the indicated p21 mutants. U2OS and HFL1 cells were transduced and fixed 48 h later. At least 500 nuclei/sample were analyzed. N = 2 (Statistics: one-way ANOVA, Tukey post test). C Representative images of DAPI-stained HFL1 cells transduced with either EV or sPIRp21 particles. 48 h later, cells were either mock treated (NT) or treated with UV (5 J/m2), CDDP (1 μM) or Chk1i (Gö6976 0.25 µM) and fixed 6 days later. D Cell number (mean ± SD) expressed as fold changes with respect to the EV transduced, mock treated (NT) HFL1 cells shown in (C). The total cell number in 3 wells from a 96-well plate was quantified for each condition. N = 2 (Statistics: one-way ANOVA, Tukey post test, samples were compared within each treatment). E Cell number (mean ± SD) relative to untreated HFL1 cells transduced with either EV, sPIRp21 or sPIRp21ΔP. 6 days after the treatment with the indicated UV, CDDP or Chk1i doses, the total cell number in 3 wells from a 96-well plate was counted for each condition. N = 2 (Statistics: one-way ANOVA, Tukey post test). The same source data used in D was used here.
