15-deoxy-[[DELTA].sup.12,14]-prostaglandin [J.sub.2] induces apoptosis and upregulates SOCS3 in human thyroid cancer cells

• Published in: PPAR research
• Main Authors: Trindade-da-Silva, Carlos Antonio, Reis, Carolina Fernandes, Vecchi, Lara, Napimoga, Marcelo Henrique, Sperandio, Marcelo, Colombo, Bruna Franca Matias, Alves, Patricia Terra, Ward, Laura Sterian, Ueira-Vieira, Carlos, Goulart, Luiz Ricardo
• Format: Journal Article
• Language: English
• Published: John Wiley & Sons, Inc 01.01.2016
• Subjects: Apoptosis; Care and treatment; Cell receptors; Health aspects; Prostaglandins; Thyroid cancer
• ISSN: 1687-4757
• DOI: 10.1155/2016/4106297

The cyclopentenone prostaglandin 15-deoxy-[[DELTA].sup.12,14]-prostaglandin [J.sub.2] ([15d-PGJ.sub.2]) is a natural ligand of peroxisome proliferator-activated receptor gamma (PPAR-[gamma]) and a potential mediator of apoptosis in cancer cells. In the present study, we evaluated the effect of [15d-PGJ.sub.2] inhuman thyroid papillary carcinoma cells (TPC-1) using different doses of [15d-PGJ.sub.2] (0.6 to 20 [micro]M) to determine [IC.sub.50] (9.3 [micro]M) via the MTT assay. The supernatant culture medium of the TPC-1 cells that was treated either with [15d-PGJ.sub.2] or with vehicle (control) for 24 hours was assessed for IL-6 secretion via CBA assay. RT-qPCR was used to evaluate mRNA expression of IL6, SOCS1, SOCS3, and STAT3. TPC-1 cells treated with [15d-PGJ.sub.2] decreased the secretion and expression of IL-6 and STAT3, while it increased SOCS1 and SOCS3. Overall, we demonstrated that [15d-PGJ.sub.2] downregulated IL-6 signaling pathway and led TPC-1 cells into apoptosis. In conclusion, [15d-PGJ.sub.2] shows the potential to become a new therapeutic approach for thyroid tumors.