Skip to main content
Figure 3 | Molecular Cancer

Figure 3

From: cAMP signaling inhibits radiation-induced ATM phosphorylation leading to the augmentation of apoptosis in human lung cancer cells

Figure 3

Gαs augmented radiation-induced apoptosis by inhibiting ATM activation in lung cancer cells. (A) Effects of Gαs on radiation-induced cleavage of caspase-3 and PARP in H1299 cells. (B) Effects of Gαs on radiation-induced early apoptosis in H1299 cells. (C) Effects of ATM knockdown on radiation-induced cleavage of caspase-3 and PARP in H1299 cells. (D) Effect of chloroquine on radiation-induced apoptosis in H1299 cells. (E) Effect of GαsQL on radiation-induced cleavage of caspase 3 and PARP in A549 cells. (F) Effects of Gαs on radiation-induced early apoptosis in A549 cells. The cells were irradiated with γ-rays (5 Gy) and incubated for 30 min for analysis of ATM phosphorylation. For analysis of apoptosis, the cells were pretreated with 10 μM KU55933 or DMSO for 30 min, irradiated with γ-rays (10 Gy) and incubated for 24 h. To determine the effects of chloroquine, the cells were pretreated with 20 μg/ml chloroquine for 4 h before irradiation; the culture medium was replaced with fresh medium at 1 h after irradiation. The cells were incubated for an additional 23 h, and then harvested and analyzed by western blotting or flow cytometry after staining with annexin V and propidium iodide (PI). The histograms present the ratio of annexin V-positive but propidium iodide-negative cells, and asterisks (*) on the histograms indicate a statistically significant difference from the vector-transfected control cells (p < 0.05, Mann–Whitney U test).

Back to article page