Up-regulation of miR-146b and Down-regulation of miR-200b Contribute to the Cytotoxic Effect of Histone Deacetylase Inhibitors onras-Transformed Thyroid Cells | Zendy

Eleonora Borbone | Zendy; Mariarosaria De Rosa | Zendy; Diletta Siciliano | Zendy; Lucia Altucci | Zendy; Carlo M. Croce | Zendy; Alfredo Fusco | Zendy

Open Access

Up-regulation of miR-146b and Down-regulation of miR-200b Contribute to the Cytotoxic Effect of Histone Deacetylase Inhibitors onras-Transformed Thyroid Cells

Author(s) -

Eleonora Borbone,

Mariarosaria De Rosa,

Diletta Siciliano,

Lucia Altucci,

Carlo M. Croce,

Alfredo Fusco

Publication year - 2013

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2012-4092

Subject(s) - vorinostat , apoptosis , histone deacetylase , cancer research , microrna , cytotoxic t cell , proteasome , histone deacetylase inhibitor , chemistry , microbiology and biotechnology , ubiquitin , cell growth , histone , biology , biochemistry , gene , in vitro

Histone deacetylase inhibitors (HDACis) are anticancer agents that inhibit tumor cell growth and/or survival. However, their mechanism of action remains largely undefined. Recently, we have demonstrated that HDACis induce apoptosis in a model of rat thyroid cells transformed by the v-ras-Ki oncogene (FRTL-5 v-ras-Ki). The stabilization of TNF-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.

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