http://www.cnr.it/ontology/cnr/individuo/prodotto/ID208307
Up-regulation of miR-146b and down-regulation of miR-200b contribute to the cytotoxic effect of Histone deacetylase inhibitors on ras-transformed thyroid cells. (Articolo in rivista)
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- Label
- Up-regulation of miR-146b and down-regulation of miR-200b contribute to the cytotoxic effect of Histone deacetylase inhibitors on ras-transformed thyroid cells. (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Alternative label
Borbone E, De Rosa M, Siciliano D, Altucci L, Croce CM, Fusco A. (2013)
Up-regulation of miR-146b and down-regulation of miR-200b contribute to the cytotoxic effect of Histone deacetylase inhibitors on ras-transformed thyroid cells.
in The Journal of clinical endocrinology and metabolism
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Borbone E, De Rosa M, Siciliano D, Altucci L, Croce CM, Fusco A. (literal)
- Rivista
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Istituto di Endocrinologia ed Oncologia Sperimentale-CNR c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli \"Federico II\" and SEMM--European School of Molecular Medicine, Naples, Italy;
Dipartimento di Patologia Generale, Seconda Università degli Studi di Napoli, Italy;
Department of Molecular Virology, Immunology, and Medical Genetics, CCC, OH State University, Columbus, OH;
Istituto di Genetica e Biofisica 'Adriano Buzzati Traverso', Naples, Italy (literal)
- Titolo
- Up-regulation of miR-146b and down-regulation of miR-200b contribute to the cytotoxic effect of Histone deacetylase inhibitors on ras-transformed thyroid cells. (literal)
- Abstract
- Context:Histone deacetylase inhibitors (HDACis) are anti-cancer agents that inhibit tumor cell growth and/or survival. However, their mechanism of action remains largely undefined. Recently, we have demonstrated that HDAC inhibitors induce apoptosis in a model of rat thyroid cells transformed by the v-ras-Ki oncogene (FRTL-5 v-ras-Ki). The stabilization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein, due to its reduced ubiquitination and proteasome degradation, accounts for the apoptotic effect induced specifically by Suberoylanilide hydroxamic acid (SAHA, Vorinostat) in the v-ras-Ki-thyroid transformed cells.Objective:The aim of this work was to investigate whether SAHA may induce its cytotoxic effects also deregulating microRNA expression levels.Design:We analyzed the miRNA expression profile of the thyroid transformed cells FRTL-5 v-ras-Ki upon SAHA treatment.Results:Here, we report that SAHA induces the down-regulation of 18 and the up-regulation of 11 miRNAs with a fold-change higher than 2 in the transformed cells. Then, we focus on the miR-146b and miR-200b, respectively up-regulated and down-regulated by SAHA. We show that both these miRNAs target genes coding for proteins with a critical role in proteasome composition and ubiquitin degradation.Conclusion:These results suggest a role of miRNA deregulation in TRAIL protein stabilization responsible for SAHA-induced apoptotic effect in thyroid transformed cells. (literal)
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