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MiR-599 serves a suppressive role in anaplastic thyroid cancer by activating the T-cell intracellular antigen
Anaplastic thyroid cancer (ATC) has a mean survival time of 6 months and accounts for 1–2% of all thyroid tumors. Understanding the underlying molecular mechanisms of carcinogenesis and progression in ATC would contribute to the identification of novel therapeutic targets. A previous study revealed...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755273/ https://www.ncbi.nlm.nih.gov/pubmed/31555352 http://dx.doi.org/10.3892/etm.2019.7864 |
Sumario: | Anaplastic thyroid cancer (ATC) has a mean survival time of 6 months and accounts for 1–2% of all thyroid tumors. Understanding the underlying molecular mechanisms of carcinogenesis and progression in ATC would contribute to the identification of novel therapeutic targets. A previous study revealed that microRNA (miR)-599 was associated with tumor initiation and development in certain types of cancer. However, the specific functions and mechanisms of miR-599 in ATC are poorly understood. The objective of the present study was to identify its expression, function and molecular mechanism in ATC. The expression levels of miR-599 in 10 pairs of surgical specimens and human ATC cell lines were examined by reverse transcription-quantitative polymerase chain reaction. Function assays illustrated that miR-599 overexpression not only suppressed KAT-18 cell viability, proliferation and metastasis in vitro and decreased tumor growth in the tumor xenograft model but also induced cell apoptosis. Furthermore, T-cell intracellular antigen (TIA1), a tumor suppressor, was confirmed as a direct target of miR-599. It was demonstrated that TIA1 silencing rescued the inhibitory effect of migration and invasion induced by the overexpression of miR-599 in KAT-18 cells. In conclusion, the present study revealed that miR-599 inhibited ATC cell growth and metastasis via activation of TIA1. Therefore miR-599 may be a novel molecular therapeutic target for ATC. |
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