ArticleJournal of endocrinological investigation2018
The AMPK-activator AICAR in thyroid cancer: effects on CXCL8 secretion and on CXCL8-induced neoplastic cell migration.
Article in Journal of endocrinological investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Selective anti-CXCR2 receptor blockade by AZD5069 inhibits CXCL8-mediated pro-tumorigenic activity in human thyroid cancer cells in vitro.Journal of endocrinological investigation · 2025Article
- Investigating the Effects of Morin and Aminoimidazole Carboxamide Ribonucleotide on the AMPK/mTOR/ULK1 Signaling Pathway in Breast Cancer Cell Line (MCF-7).Advanced biomedical research · 2025Article
- Vitamin C in the Management of Thyroid Cancer: A Highway to New Treatment?Antioxidants (Basel, Switzerland) · 2024Review
- Biomarkers related to m6A and succinic acid metabolism in papillary thyroid carcinoma.BMC medical genomics · 2024Article
- AMPK Alchemy: Therapeutic Potentials in Allergy, Aging, and Cancer.Biomolecules & therapeutics · 2024Review
- Long non-coding RNA ACTA2-AS1 suppresses metastasis of papillary thyroid cancer via regulation of miR-4428/KLF9 axis.Clinical epigenetics · 2024Article
- The role of AMPK in cancer metabolism and its impact on the immunomodulation of the tumor microenvironment.Frontiers in immunology · 2023Review
- A Multi-enzyme Cascade for the Biosynthesis of AICA Ribonucleoside Di- and Triphosphate.Chembiochem : a European journal of chemical biology · 2022Article
- Construction of a Tumor Immune Microenvironment-Related Prognostic Model in BRAF-Mutated Papillary Thyroid Cancer.Frontiers in endocrinology · 2022Article
- Correlation analysis of survivin, ING4, CXCL8 and VEGF expression in prostate cancer tissue.American journal of translational research · 2021Article
- CD73-dependent adenosine dampens interleukin-1β-induced CXCL8 production in gingival fibroblasts: Association with heme oxygenase-1 and adenosine monophosphate-activated protein kinase.Journal of periodontology · 2020Article
- Angustoline Inhibited Esophageal Tumors Through Regulating LKB1/AMPK/ELAVL1/LPACT2 Pathway and Phospholipid Remodeling.Frontiers in oncology · 2020Article
- Immune Microenvironment of Thyroid Cancer.Journal of Cancer · 2020Review
- The multifaceted anti-cancer effects of BRAF-inhibitors.Oncotarget · 2019Review
- The anti-cancer effects of phenformin in thyroid cancer cell lines and in normal thyrocytes.Oncotarget · 2019Article
- Identification and Validation of Core Genes Involved in the Development of Papillary Thyroid Carcinoma via Bioinformatics Analysis.International journal of genomics · 2019Article
- Role of Chemokines in Thyroid Cancer Microenvironment: Is CXCL8 the Main Player?Frontiers in endocrinology · 2018Review
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe 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).
methodsThe 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.
resultsAICAR dose dependently inhibited the basal secretion of CXCL8 in TPC-1 (F = 4.26; p < 0.007) and BCPAP (F = 6.75; p < 0.0001) but not in NHT. TNFα-induced CXCL8 secretion was dose dependently reduced by AICAR in NHT (F = 9.99; p < 0.0001), TPC-1 (F = 9.25; p < 0.0001) and BCPAP (F = 6.82; p < 0.0001). AICAR significantly reduced the basal migration of TPC-1 and BCPAP but not of NHT.
conclusionsCXCL8-induced cell migration was inhibited in NHT, TPC-1 and BCPAP. This is the first demonstration of the inhibition of CXCL8 secretion exerted by AICAR in TPC-1 and BCPAP indicating that the anti-cancer properties of AICAR are, at least in part, mediated by its ability to reduce the pro-tumorigenic effects of CXCL8.
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