Fig. 1. Cell-type-specific modulation of γ-ray-induced DNA damage and apoptosis by cAMP signaling. (A) Effects of pretreatment with isoproterenol and PGE2 on γ-H2AX formation following γ-ray irradiation in human malignant melanoma cells. The empty bars present SK-MEL-2 cells, and the filled bars present SK-MEL-28 cells. (B) Effects of PGE2 and isoproterenol on γ-H2AX formation following γ-ray irradiation in human uterine cervical cancer cells. The empty bars present HeLa cells, and the filled bars present SiHa cells. (C) Effects of PGE2 and isoproterenol on γ-H2AX formation following γ-ray irradiation of human non-small cell lung cancer cells. The empty bars present H1299 cells, and the filled bars present A549 cells. The cells pretreated with 1 μM isoproterenol (ISO) or 20 μM PGE2 for 30 minutes were irradiated with γ-rays (5 Gy) and collected with a cell scraper after 1 h for analysis by western blotting. (D, E, F) PGE2 effects on the cleavage of PARP and caspase-9 following γ-ray irradiation in SK-MEL-28 cells (D), HeLa cells (E), and A549 cells (F). The cells pretreated with PGE2 (20 μM, 30 minutes) were irradiated with γ-rays (5 Gy) and collected with a cell scraper after 24 hours (A549 and HeLa) or 48 hours (SK-MEL-28) for analysis by western blotting. The empty bars shows cleaved PARP, and the filled bars shows cleaved caspase-9. The means ± standard error calculated from the three independent experiments were presented as columns. The asterisk (*) denotes statistically significant differences compared with the respective control (P ≤ 0.05, Mann-Whitney U test).