15-deoxy-delta(12-14)-prostaglandin-j2 has been researched along with Thyroid-Neoplasms* in 1 studies
1 other study(ies) available for 15-deoxy-delta(12-14)-prostaglandin-j2 and Thyroid-Neoplasms
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15-Deoxy-delta12,14-prostaglandin J2 induces apoptosis of a thyroid papillary cancer cell line (CG3 cells) through increasing intracellular iron and oxidative stress.
Treatment of carcinoma cell lines with 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), a natural ligand of the peroxisome proliferator-activated receptor-gamma, has been reported to induce apoptosis and/or inhibit proliferation. In this study, we investigated the cytotoxic effect and the action mechanisms of 15d-PGJ2 in a thyroid papillary cancer cell line, CG3. The results indicate that 15d-PGJ2 caused cytotoxicity and increased the amount of intracellular reactive oxygen species (ROS) in these cells. Mitochondrial oxidative phosphorylation inhibitors (carbonyl cyanide m-chloro-phenylhydrazone, oligomycin, cyclosporin A and rotenone), NADPH oxidase inhibitor (diphenyleneiodonium), xanthine oxidase inhibitor (allopurinol) and NO synthase inhibitor (N-monomethyl-L-arginine acetate) did not reduce the generation of ROS. However, catalase, N-acetyl-cysteine and the iron chelator desferri-oxamine decreased the intracellular ROS of 15d-PGJ2-treated CG3 cells. Furthermore, 15d-PGJ2 enhanced the accumulation of iron in the CG3 cells. These data suggest that 15d-PGJ2 induces the generation of ROS by enhancing the accumulation of intracellular iron and that the increased oxidative stress may cause apoptosis of CG3 cells. Topics: Apoptosis; Carcinoma, Papillary; Caspases; Cell Count; Cell Survival; Enzyme Activation; Humans; Immunologic Factors; Indicators and Reagents; Iron; Iron Chelating Agents; Lipid Peroxidation; Oxidative Stress; Prostaglandin D2; Reactive Oxygen Species; Stimulation, Chemical; Thyroid Neoplasms; Tumor Cells, Cultured | 2002 |