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. 2012 Jun 25;287(34):29075–29087. doi: 10.1074/jbc.M112.365494

FIGURE 4.

FIGURE 4.

CDK4/6 inhibition reduces Rad51 protein levels, but does not modify the rate of DNA damage repair in breast cancer cells treated with γ-irradiation. A, quantification of phospho-γ-H2AX foci over 24 h post IR in RB-proficient breast cancer cells treated with 2 Gy IR, 500 nm PD0332991 for 24 h followed by 2 Gy IR (PD-pretreatment) or 500 nm PD0332991 at the time of IR (Concurrent). Data are represented as the average number of phospho-γ-H2AX foci per cell as visualized by immunofluorescence. B, (left) representative immunofluorescence images of Rad51 protein among treatments described in A. RB-deficient MDA-MB-468 cells are included for comparison. Right, quantification of Rad51 foci and average Rad51 foci size 24 h post IR exposure. C, immunoblot analysis examining Rad51 protein levels and RB/E2F target gene product response in RB-proficient and RB-deficient breast cancer cell lines after treatment with 500 nm PD0332991, 2 Gy IR or 24 h 500 nm PD0332991 treatment followed by 2 Gy IR (PD-pretreat). Lamin B served as a loading control. D, immunoblot analysis of Rad51 protein levels in matched RB-proficient and RB-knockdown breast cancer cells after 500 nm PD0332991 treatment, 2 Gy IR or exposure to 500 nm PD0332991 24 h prior to IR (PD-pretreatment).