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Mediators of Inflammation
Volume 2016, Article ID 8512417, 7 pages
Research Article

Effect of Interferon-γ on the Basal and the TNFα-Stimulated Secretion of CXCL8 in Thyroid Cancer Cell Lines Bearing Either the RET/PTC Rearrangement Or the BRAF V600e Mutation

1Unit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri I.R.C.C.S., Laboratory for Endocrine Disruptors and Chair of Endocrinology University of Pavia, 27100 Pavia, Italy
2Department of Biopharmaceutics and Clinical Pharmacy, The University of Jordan, Amman 11937, Jordan
3Allergy and Immunology Unit, Fondazione Salvatore Maugeri I.R.C.C.S., 27100 Pavia, Italy
4Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy
5Biotechnology Research Laboratories, I.R.C.C.S., Policlinico San Matteo Foundation, 27100 Pavia, Italy
6Department of Biomedical Engineering, Tufts University, Medford, MA 02155, USA

Received 18 May 2016; Revised 1 July 2016; Accepted 10 July 2016

Academic Editor: Carolina T. Piñeiro

Copyright © 2016 Mario Rotondi 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.


CXCL8 displays several tumor-promoting effects. Targeting and/or lowering CXCL8 concentrations within the tumor microenvironment would produce a therapeutic benefit. Aim of this study was to test the effect of IFNγ on the basal and TNFα-stimulated secretion of CXCL8 in TCP-1 and BCPAP thyroid cancer cell lines (harboring RET/PTC rearrangement and BRAF V600e mutation, resp.). Cells were incubated with IFNγ (1, 10, 100, and 1000 U/mL) alone or in combination with TNF-α (10 ng/mL) for 24 hours. CXCL8 and CXCL10 concentrations were measured in the cell supernatants. IFNγ inhibited in a dose-dependent and significant manner both the basal (ANOVA F: 22.759; ) and the TNFα-stimulated (ANOVA F: 15.309; ) CXCL8 secretions in BCPAP but not in TPC-1 cells (NS). On the other hand, IFNγ and IFNγ + TNF-α induced a significant secretion of CXCL10 in both BCPAP () and TPC-1 () cells. Transwell migration assay showed that (i) CXCL8 increased cell migration in both TPC-1 and BCPAP cells; (ii) IFNγ significantly reduced the migration only of BCPAP cells; and (iii) CXCL8 reverted the effect of IFNγ. These results constitute the first demonstration that IFNγ inhibits CXCL8 secretion and in turn the migration of a BRAF V600e mutated thyroid cell line.