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. 2016 Sep 17;7(43):69976–69990. doi: 10.18632/oncotarget.12099

Figure 4. RAD51-dependent HR is a crucial mediator of HT29 survival after irradiation.

Figure 4

(A) Immunofluorescence of RAD51 and γ-H2AX foci formation post IR. HT29 cells were seeded onto cover slips and treated with a single 6 Gy dose of γ-rays. 24 h after IR, cells were formalin fixed, permeabilized, and stained with RAD51 and γ-H2AX antibodies. (B) Western blots showing the effect of RAD51 knockdown on the damage marker, γ-H2AX. (C) Western blots confirming the efficiency of the two tested RAD51 siRNAs. (D) Clonogenic surviving fractions of scrambled/RAD51 siRNA treated HT29 cells showing increased cell killing and induced radiosensitivity of the radioresistant HT29 cells after RAD51 knockdown. Cells were exposed to a single 6 Gy dose of γ-rays, and the surviving fractions were calculated by dividing the number of colonies counted by the corresponding number of cells seeded as described in “Materials and Methods.”