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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Radiother Oncol. 2016 Sep 22;121(1):162–168. doi: 10.1016/j.radonc.2016.08.029

Fig. 3.

Fig. 3

PU-H71 affects the HR and NHEJ repair pathway in human cancer cells. (A) HeLa-SQ5 cells were pretreated with 1 µMPU-H71 for 24 h, and irradiated with 4 Gy carbon ions. At indicated times after irradiation, cells were collected and total cellular proteins were immunoblotted with RAD51 and GAPDH antibodies. GAPDH was used as loading control. Numbers below the bands correspond to the fold changes normalized to non-drug treated and non-irradiated control cells. (B) HeLa-SQ5 cells pretreated with PU-H71 (1 µM) or DMSO were fixed at indicated times after 2 Gy carbon ion irradiation. Cells were incubated with anti-RAD51 and anti-Cyclin B, and the number of RAD51 foci per nucleus was counted in Cyclin-B stained cells. Data represent mean ± SEM of three independent experiments. * indicates p < 0.05. (C) To assess the effects of PU-H71 on DNA-PKcs activation we collected A549 cells and H1299 cells 2 h after 2 Gy carbon ion irradiation and total cellular proteins were immunoblotted with antibodies against phosphorylated DNA-PKcs (phospho S2056 and phospho T2609), EGFR, phosphorylated ERK, and GAPDH. GAPDH was used as loading control.