Death receptor regulation and celecoxib-induced apoptosis in human lung cancer cells

chemopreventive and therapeutic activities toward lung can-cer and other epithelial malignancies. Celecoxib can induce apoptosis in various cancer cell lines through a mechanism that is independent of its cyclooxygenase 2 inhibitory activity but is otherwise largely uncharacterized. We investigated the mechanism of celecoxib-induced apoptosis further. Methods: All experiments were conducted in human non-small-cell lung carcinoma (NSCLC) cell lines; results in celecoxib-treated and untreated cells were compared. Cell survival was assessed with a sulforhodamine B assay. Apoptosis was as-sessed by DNA fragmentation with an enzyme-linked immu-nosorbent assay, by terminal deoxynucleotidyltransferase-mediated dUTP nick-end-labeling (TUNEL) assay, and by western blot analysis of caspase activation. Death receptor gene and protein expression was detected by northern an