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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Mol Cancer Res. 2017 Jan 10;15(3):269–280. doi: 10.1158/1541-7786.MCR-16-0227-T

Figure 4. Mismatch repair is required for cisplatin-induced apoptosis in WT cells.

Figure 4

A. DLD1 cells deficient in MSH6 (−MSH6; dashed lines, open symbols) or complemented with MSH6 (+MSH6; solid lines, filled symbols) expressing WT or P242R Pol β or empty vector, were treated with various concentrations of cisplatin (0-6.25 μM). B. HCT116 cells deficient in MLH1 (−MLH1; dashed lines, open symbols) or complemented with MLH1 (+MLH1; solid lines, filled symbols) were treated with various concentrations of cisplatin (0-12.5 μM). A-B. Clonogenic survival assays were performed. C-D. DLD1 cells deficient in MSH6 (−MSH6; open bars) or complemented with MSH6 (+MSH6; filled bars) were treated with 6.25 μM cisplatin and allowed to recover for 0-48 h (C) or 0 and 96 h (D). C. Double-strand breaks were measured by staining with γH2AX antibody using flow cytometry. D. Apoptotic cells were measured by staining with Annexin V antibody. Data are presented as the ratio of apoptotic cells in cisplatin-treated cells vs untreated cells for each cell line. All data are presented as mean ± SEM (n = 3). Two-way ANOVA with Bonferroni’s post hoc test (C) or two-tailed t-tests (D) were performed to determine significance.