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  • Author: Vincenza Leone x
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Vincenza Leone Istituto di Endocrinologia ed Oncologia Sperimentale-CNR, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli ‘Federico II', Naples, Italy

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Concetta Langella Istituto di Endocrinologia ed Oncologia Sperimentale-CNR, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli ‘Federico II', Naples, Italy

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Francesco Esposito Istituto di Endocrinologia ed Oncologia Sperimentale-CNR, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli ‘Federico II', Naples, Italy

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Marco De Martino Istituto di Endocrinologia ed Oncologia Sperimentale-CNR, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli ‘Federico II', Naples, Italy

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Myriam Decaussin-Petrucci Department of Pathology, Lyon Sud Hospital Center, Hospices Civils de Lyon, Lyon, France

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Gennaro Chiappetta Istituto Nazionale per lo Studio e la Cura dei Tumori ‘Fondazione Giovanni Pascale', IRCCS, Naples, Italy

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Antonio Bianco Dipartimento di Sanità Pubblica, Università di Napoli Federico II, Naples, Italy

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Alfredo Fusco Istituto di Endocrinologia ed Oncologia Sperimentale-CNR, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli ‘Federico II', Naples, Italy
Instituto Nacional de Cancer (INCA), Rio de Janeiro, Brazil

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We have previously studied the function of microRNAs (miRNAs) in thyroid cells using the differentiated rat thyroid PC Cl 3 cells that need thyrotropin (TSH) for their growth. The miRNA expression profile examination allowed the detection of a set of miRNAs downregulated and upregulated by TSH. Here, we first demonstrated that upregulation of miR-130b-3p occurs through a protein kinase A-cAMP-responsive element binding protein (CREB)-dependent mechanism. Then, we analyzed its expression in human thyroid follicular adenomas, where a constitutive CREB activation is frequently present. miR-130b-3p results in upregulation with a high fold-change in most thyroid follicular adenomas. Then, we identified CCDC6, coding for a protein that interacts with CREB1 leading to the transcriptional repression of CREB1 target genes, as a target of this miRNA. The targeting of CCDC6 by miR-130b-3p likely accounts for the mechanism by which its upregulation contributes to the development of thyroid adenomas increasing CREB1 activity.

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