Research Paper Volume 12, Issue 21 pp 21758—21776
Caspase-3 knockout attenuates radiation-induced tumor repopulation via impairing the ATM/p53/Cox-2/PGE2 pathway in non-small cell lung cancer
Figure 7. Schematic illustration of the proposed mechanism of radiation-induced tumor repopulation in NSCLC. Radiation-induced DNA double-strand breaks (DSBs) activate the DNA damage response (DDR) and caspase-3. Activated caspase-3 regulates the EndoG nuclear translocation and thus participates in the DDR by regulating ATM/p53 signaling, which activates the Cox-2/PGE2 axis in dying NSCLC cells, consequently enhancing the proliferation of living tumor cells.