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. 2014 Jun;85(6):866–876. doi: 10.1124/mol.113.090688

Fig. 2.

Fig. 2.

Blocking Rad51 upregulation resensitizes prostate cancer cells to drug-induced DNA damage and apoptosis under hypoxia. (A) Nuclear foci formation of Rad51 and BRCA1 as detected by immunofluorescence in normoxic and hypoxic PC3 cells either untreated (control) or treated with 0.1 µM SN38 for 4 hours. (B) Western blots of DNA ligase IV and DNA-dependent protein kinase (DNA-PK) in untreated controls and SN38-treated cells under normoxic and hypoxic conditions. (C) Western blots comparing the Rad51 and γ-H2AX levels with and without SN38 treatment in untransfected, mock siRNA-transfected and RAD51 siRNA-transfected PC3 cells under hypoxia. (D) Percentage of apoptosis as detected by flow cytometry in siRNA-transfected as well as untransfected PC3 cells under hypoxia. β-Actin was used as the loading control. Three replicates were performed for each experiment. Each column represents the mean and S.E.M. of three independent experiments. *P < 0.05.