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 3. Caspase-3-dependent PGE2 production in dying NSCLC cells induces tumor repopulation. (A) Western blot analysis of Cox-2 levels at various time intervals after 8 Gy irradiation of wild-type and Casp3 KO NSCLC cells (***p<0.001, one-way analysis of variance [ANOVA], n = 3). (B) Quantitative polymerase chain reaction (qPCR) analysis of Cox-2 in wild-type and Casp3 KO NSCLC cells at indicated times after 8 Gy irradiation (*p<0.05, **p<0.01, ***p<0.001, one-way ANOVA, n = 3). (C) Levels of prostaglandin E2 (PGE2) in culture supernatants of wild-type and Casp3 KO NSCLC cells at 48 h after 8 Gy irradiation were measured using enzyme-linked immunosorbent assay (ELISA) (***p<0.001, one-way ANOVA, n = 3). (D) A selective Cox-2 inhibitor, celecoxib, abrogated the pro-proliferation effects of dying NSCLC cells on Fluc cells in a dose-dependent manner (*p<0.05, ***p<0.001, NS = not significant, one-way ANOVA, n = 4).