Figure 3.

DNA damage binding protein 2 (DDB2) depletion downregulates Rad51, leading to defective homologous recombination (HR) repair. A‐C, DDB2‐depleted SUM159 cells with or without Rad51 upregulation were exposed to 150 μmol/L poly ADP‐ribose polymerase inhibitor (PARPi) for 24 h, and apoptosis was measured by flow cytometry. Data are shown as the mean of 3 independent experiments ± SEM. **P < .01. D‐F, DDB2‐overexpressing MDA‐MB‐231 cells with or without Rad51 silencing were exposed to 150 μmol/L PARPi for 24 h, and apoptosis was measured by flow cytometry. Data are shown as the mean of 3 independent experiments ± SEM. **P < .01. G, Immunofluorescent staining of DDB2 and Rad51 in SUM159 cells with DDB2 depletion alone or both DDB2 depletion and PARPi treatment. H, Immunofluorescent staining of DDB2 and Rad51 in MDA‐MB‐231 with DDB2 upregulation alone or both DDB2 upregulation and PARPi treatment. I,J, SUM‐159 cells carrying the recombination substrate (DR‐GFP) were transfected with expression vectors for DDB2 shRNA or both DDB2 shRNA and Rad51 shRNA. The I‐SceI expression plasmid was transiently transfected, and the GFP‐positive cells were analyzed 48 h later by flow cytometry. K,L, MDA‐MB‐231 cells carrying DR‐GFP were transfected with expression vectors for DDB2 or both DDB2 RNA and Rad51 shRNA