Fig. 1

MRE11A deficiency sensitizes cells to MNNG treatment. A HeLa cells were transfected with two different siRNAs targeting MRE11A and exhibited abnormal morphology and reduced survival 72 h after 200 nM MNNG treatment. The survival rate was the percentage of surviving cells to parallel cells treated only with O6-benzylguaine and DMSO in each group, and cells with MLH1 deficiency were used as a positive control. B MRE11A knockdown cells were treated with MNNG and seeded in triplicate in six-well plates, and after approximately 2 weeks, the cells were stained with Crystal Violet, and the colonies with ≥ 200 cells were counted. The survival rate was the percentage of surviving clones in parallel wells treated only with DMSO in each group, and cells with MLH1 deficiency were used as a positive control. C The growth rates of control cells and MRE11A knockdown cells were measured in 96-well plates with CCK8 reagents. D Western blotting showed no significant changes in the protein levels of MSH2 and MLH1 in MRE11A knockdown cells. E Representative flow cytometry pictures of scatter plots of PI versus Annexin V staining of the siNC control, MRE11A and MLH1 knockdown cells 72 h after 200 nM MNNG treatment. The right graph shows the statistical analysis of the left flow cytometry data, quantification, and comparison of the proportions of apoptotic cells in each group. The % apoptosis was calculated as the % apoptosis of cells with 200 nM MNNG minus that with only DMOS treatment. All data were analyzed with an unpaired two-tailed Student’s t test. Data are shown as mean ± SD, n = 3, *P < 0.05, **P < 0.01, ***P < 0.001