CircRTN1 acts as a miR-431-5p sponge to promote thyroid cancer progression by upregulating TGFA.
Hormones (Athens)
; 21(4): 611-623, 2022 Dec.
Article
em En
| MEDLINE
| ID: mdl-35804263
PURPOSE: This study aimed to explore the role and underlying mechanism of circular RNA (circRNA) reticulon 1 (circRTN1) in thyroid cancer (TC). METHODS: The expression levels of circRTN1, microRNA-431-5p (miR-431-5p), and transforming growth factor-alpha (TGFA) mRNA were measured by quantitative real-time PCR (qRT-PCR). Cell proliferation was evaluated using colony formation and 5-ethynyl-2'-deoxyuridine (EdU) assays. Cell apoptosis was analyzed using flow cytometry. Cell migration and invasion were measured using the transwell assay. The protein levels of ki-67, Bax, matrix metalloproteinase 2 (MMP-2), and TGFA were detected using Western blot assay. The interaction between miR-431-5p and circRTN1 or TGFA was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The effect of circRTN1on TC in vivo was explored via xenograft tumor assay. RESULTS: The expression of circRTN1 was increased in TC tissues and cells. Knockdown of circRTN1 suppressed TC cell proliferation, migration, and invasion, and increased cell apoptosis. MiR-431-5p was a target of circRTN1, and miR-431-5p downregulation reversed the role of circRTN1 knockdown in TC cells. TGFA was identified as a direct target of miR-431-5p, and miR-431-5p exerted the anti-tumor role in TC cells by downregulating TGFA. Moreover, circRTN1 sponged miR-431-5p to regulate TGFA expression. Furthermore, circRTN1 knockdown inhibited tumor growth in vivo. CONCLUSION: CircRTN1 acted as a cancer-promoting circRNA in TC by regulating the miR-431-5p/TGFA axis, providing a potential therapeutic strategy for TC treatment.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Glândula Tireoide
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Fator de Crescimento Transformador alfa
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MicroRNAs
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RNA Circular
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article