The AMPK-activator AICAR in thyroid cancer: effects on CXCL8 secretion and on CXCL8-induced neoplastic cell migration
Autor: | Oriana Awwad, Marco Denegri, Vittorio Abbonante, Laura Croce, S. Massara, Alessandra Balduini, Patrizia Pignatti, C. A. Di Buduo, Francesca Coperchini, Luca Chiovato, Mario Rotondi |
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Rok vydání: | 2018 |
Předmět: |
musculoskeletal diseases
0301 basic medicine medicine.medical_specialty Endocrinology Diabetes and Metabolism Thyroid Gland Metastasis 03 medical and health sciences 0302 clinical medicine Endocrinology Cell Movement Internal medicine Cell Line Tumor medicine Humans Secretion Interleukin 8 Thyroid Neoplasms Thyroid cancer Cell Proliferation Chemistry Tumor Necrosis Factor-alpha Interleukin-8 AMPK Cell migration Ribonucleotides medicine.disease Aminoimidazole Carboxamide 030104 developmental biology 030220 oncology & carcinogenesis Cancer cell Neoplastic cell |
Zdroj: | Journal of endocrinological investigation. 41(11) |
ISSN: | 1720-8386 |
Popis: | The AMPK-activator AICAR recently raised great interest for its anti-cancer properties. With specific regard to thyroid cancer, AICAR reduces cancer cell growth, invasion and metastasis. CXCL8, a chemokine with several recognized tumorigenic effects, is abundantly secreted in thyroid cancer microenvironment. The aim of this study was to investigate if AICAR could inhibit the basal and the TNFα-induced CXCL8 secretion in normal human thyroid cells (NHT) and in thyroid cancer cell lines TPC-1 and BCPAP (RET/PTC and BRAFV600e mutated, respectively). The effect of AICAR on basal and CXCL8-induced cell migration was assessed. Cells were incubated with AICAR (0.05, 0.5, 1, 2 mM) alone or in combination with TNF-α (10 ng/ml) for 24 h. CXCL8 concentrations were measured in cell supernatants. Transwell migration assays were performed in NHT, TPC-1 and BCPAP, basally and after treatment with AICAR (2 mM) and rh-CXCL8 (50 ng/ml) alone or in combination. AICAR dose dependently inhibited the basal secretion of CXCL8 in TPC-1 (F = 4.26; p |
Databáze: | OpenAIRE |
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