MicroRNA-574-5p directly targets FOXN3 to mediate thyroid cancer progression via Wnt/ß-catenin signaling pathway.
Pathol Res Pract
; 216(6): 152939, 2020 Jun.
Article
em En
| MEDLINE
| ID: mdl-32284251
OBJECTIVE: Thyroid cancer is the most common endocrine tumor. A large number of thyroid cancer-related miRNAs have been studied and identified. However, the detailed roles of miR-574-5p in thyroid cancer remain poorly understood. This work mainly aimed to investigate the role of miR-574-5p/FOXN3 axis and its mechanism in the thyroid cancer progression. METHODS: MiR-574-5p, FOXN3, Wnt/ß-catenin pathway, and apoptosis-related markers were measured by quantitative real-time PCR (qRT-PCR) and western blotting analysis, respectively. Luciferase reporter assay was employed to validate the direct targeting of FOXN3 by miR-574-5p. MTT, flow cytometry, wound healing and transwell experiments were applied to analyze the functions of FOXN3 and miR-574-5p in thyroid cancer cells. RESULTS: Knockdown of miR-574-5p up-regulated FOXN3 expression and miR-574-5p directly targeted FOXN3 in thyroid cancer cells. Biological function experiments showed that knockdown of miR-574-5p inhibited proliferation, migration, invasion and promoted apoptosis of thyroid cancer cells. The activation of Wnt/ß-catenin pathway was suppressed by MiR-574-5p silencing. FOXN3 silencing reversed the effects of miR-574-5p inhibitor on FOXN3 level and Wnt/ß-catenin singling pathway, also reversed the effects on cell migration, proliferation, invasion and apoptosis. CONCLUSION: The miR-574-5p/FOXN3 axis is a novel molecular mechanism that promotes thyroid cancer progression, suggesting their potential for clinical therapy of thyroid cancer.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Glândula Tireoide
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Regulação Neoplásica da Expressão Gênica
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Proteínas de Ciclo Celular
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MicroRNAs
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Fatores de Transcrição Forkhead
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Via de Sinalização Wnt
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article