The AMPK-activator AICAR in thyroid cancer: effects on CXCL8 secretion and on CXCL8-induced neoplastic cell migration

Purpose 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...

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Bibliographic Details
Published in:Journal of endocrinological investigation 2018-11, Vol.41 (11), p.1275-1282
Main Authors: Awwad, O., Coperchini, F., Pignatti, P., Denegri, M., Massara, S., Croce, L., Di Buduo, C. A., Abbonante, V., Balduini, A., Chiovato, L., Rotondi, M.
Format: Article
Language:English
Subjects:
Aminoimidazole Carboxamide - analogs & derivatives
Aminoimidazole Carboxamide - pharmacology
Cell adhesion & migration
Cell Line, Tumor
Cell migration
Cell Movement - drug effects
Cell Proliferation - drug effects
Endocrinology
Humans
Interleukin-8 - metabolism
Interleukin-8 - pharmacology
Medicine
Medicine & Public Health
Metabolic Diseases
Metastases
Original Article
Ribonucleotides - pharmacology
Thyroid cancer
Thyroid Gland - pathology
Thyroid Neoplasms - metabolism
Thyroid Neoplasms - pathology
Tumor cell lines
Tumor Necrosis Factor-alpha - pharmacology
Tumor necrosis factor-α
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Summary:Purpose 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). Methods 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. Results AICAR dose dependently inhibited the basal secretion of CXCL8 in TPC-1 ( F  = 4.26; p 
ISSN:1720-8386
0391-4097
1720-8386
DOI:10.1007/s40618-018-0862-8