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PPAR Research
Volume 2016, Article ID 4106297, 8 pages
http://dx.doi.org/10.1155/2016/4106297
Research Article

15-Deoxy-Δ12,14-prostaglandin J2 Induces Apoptosis and Upregulates SOCS3 in Human Thyroid Cancer Cells

1Laboratory of Nanobiotechnology, Federal University of Uberlândia, 38400902 Uberlândia, MG, Brazil
2Laboratory of Genetics, Federal University of Uberlândia, 38400902 Uberlândia, MG, Brazil
3Hammock Laboratory of Pesticide Biotechnology, University of California Davis, Davis, CA 95616, USA
4Laboratory of Cancer Molecular Genetics, University of Campinas, 13081-970 Campinas, SP, Brazil
5Laboratory of Immunology and Molecular Biology, São Leopoldo Mandic Institute and Research Center, 13045-755 Campinas, SP, Brazil
6Department of Medical Microbiology and Immunology, University of California Davis, Davis, CA 95616, USA

Received 16 December 2015; Accepted 1 March 2016

Academic Editor: Constantinos Giaginis

Copyright © 2016 Carlos Antônio Trindade-da-Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The cyclopentenone prostaglandin 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is a natural ligand of peroxisome proliferator-activated receptor gamma (PPAR-γ) and a potential mediator of apoptosis in cancer cells. In the present study, we evaluated the effect of 15d-PGJ2 in human thyroid papillary carcinoma cells (TPC-1) using different doses of 15d-PGJ2 (0.6 to 20 μM) to determine IC50 (9.3 μM) via the MTT assay. The supernatant culture medium of the TPC-1 cells that was treated either with 15d-PGJ2 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 IL-6, SOCS1, SOCS3, and STAT3. TPC-1 cells treated with 15d-PGJ2 decreased the secretion and expression of IL-6 and STAT3, while it increased SOCS1 and SOCS3. Overall, we demonstrated that 15d-PGJ2 downregulated IL-6 signaling pathway and led TPC-1 cells into apoptosis. In conclusion, 15d-PGJ2 shows the potential to become a new therapeutic approach for thyroid tumors.