| Autor: |
Penha, Ricardo Cortez Cardoso, Sepe, Romina, De Martino, Marco, Esposito, Francesco, Pellecchia, Simona, Raia, Maddalena, del Vecchio, Luigi, Decaussin-Petrucci, Myriam, De Vita, Gabriella, Pinto, Luis Felipe Ribeiro, Fusco, Alfredo |
| Zdroj: |
Cell Cycle; 2017, Vol. 16 Issue 23, p2282-2289, 8p |
| Abstrakt: |
DICER1plays a central role in the biogenesis of microRNAs and it is important for normal development. Altered microRNA expression andDICER1dysregulation have been described in several types of tumors, including thyroid carcinomas. Recently, our group identified a new somatic mutation (c.5438A>G; E1813G) withinDICER1gene of an unknown function. Herein, we show thatDICER1is overexpressed, at mRNA level, in a significant-relative number of papillary (70%) and anaplastic (42%) thyroid carcinoma samples, whereas is drastically downregulated in all the analyzed human thyroid carcinoma cell lines (TPC-1, BCPAP, FRO and 8505c) in comparison with normal thyroid tissue samples. Conversely,DICER1is downregulated, at protein level, in PTC in comparison with normal thyroid tissues. Our data also reveals thatDICER1overexpression positively regulates thyroid cell proliferation, whereas its silencing impairs thyroid cell differentiation. The expression ofDICER1gene mutation (c.5438A>G; E1813G) negatively affects the microRNA machinery and cell proliferation as well as upregulatesDICER1protein levels of thyroid cells but has no impact on thyroid differentiation. In conclusion,DICER1protein is downregulated in papillary thyroid carcinomas and affects thyroid proliferation and differentiation, whileDICER1gene mutation (c.5438A>G; E1813G) compromises theDICER1wild-type-mediated microRNA processing and cell proliferation. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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