Fig. 2: MMC induces DSBs and shows potent killing effects in BRCA2 monoallelic and biallelic mutant tumor cells.
From: Brca2 deficiency drives gastrointestinal tumor formation and is selectively inhibited by mitomycin C
a After SNU-1, SNU-5 and HGC-27 cells were treated with the indicated drugs for 72 h, the cell viability was determined at OD570, with normalization to DMSO treatment. b Representative images of γ-H2AX and BRCA2 foci formation in BRCA2 wild-type and mutant cell lines after treated with 0.3 μM MMC for 18 h. Scale bar, 10 μm. c Representative images of γ-H2AX and RAD51 foci formation in BRCA2 wild-type and mutant cell lines after treatment with 0.3 μM MMC or vehicle for 18 h. Scale bar, 10 μm. d The quantification of γ-H2AX and BRCA2 foci formation in BRCA2 wild-type and mutant cell lines in the absence and presence of 0.3 μM MMC treatment for 18 h. e The quantification of γ-H2AX and RAD51 foci formation in BRCA2 wild-type and mutant cell lines after treatment with 0.3 μM MMC or vehicle for 18 h. f The flow cytometry data of SNU-216, SNU-1, SNU-5, and HGC-27 after treatment with 0.1% DMSO or 1 μM MMC for 24 h. g The cell-cycle phases of SNU-216, SNU-1, SNU-5, and HGC-27 were presented after treatment with 0.1% DMSO or 1 μM MMC for 24 h. h The relative S phases of SNU-216, SNU-1, SNU-5, and HGC-27 were calculated and statistical analyzed after treatment with 0.1% DMSO or 1 μM MMC for 24 h. i Single-cell electrophoresis in the indicated cell lines after treatment with 3 μM MMC or vehicle for 36 h. Scale bar, 10 μm. j Quantification of single-cell electrophoresis in indicated cell lines. k Immunoblotting analysis of γ-H2AX, PARP and cleaved-PARP in the indicated cell lines after treatment with 0.3 μM MMC for 18 h plus withdrawal for 24 h. Data represent the mean ± SD of 3–5 replicates, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
