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miRNA-218 regulates the proliferation and apoptosis of cervical cancer cells via targeting Gli3

Cervical cancer (CC) is one of the most malignant tumors that affect women. Recent studies have reported that microRNAs (miRs) serve important roles in CC. The aim of the present study was to investigate the role of miR-218 in CC and to verify its underlying mechanism. The results of reverse transcr...

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Detalles Bibliográficos
Autores principales: Zhang, Jing, Li, Shengze, Li, Yanhua, Liu, Hongli, Zhang, Yuan, Zhang, Qingsong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122525/
https://www.ncbi.nlm.nih.gov/pubmed/30210595
http://dx.doi.org/10.3892/etm.2018.6491
Descripción
Sumario:Cervical cancer (CC) is one of the most malignant tumors that affect women. Recent studies have reported that microRNAs (miRs) serve important roles in CC. The aim of the present study was to investigate the role of miR-218 in CC and to verify its underlying mechanism. The results of reverse transcription-quantitative polymerase chain reaction (RT-qPCR) revealed that miR-218 was dramatically downregulated in CC tissues and cell lines. Furthermore, the expression of Gli3 and Ki67 was measured using RT-qPCR and the results revealed that levels of these proteins were negatively correlated with miR-218 in CC tissues. The protein expression levels were determined by western blotting. Then SiHa cell line was used to investigate the mechanism of CC. Following cell transfection, cell apoptosis and cycle analyses were performed using the flow cytometry. The results revealed that miR-218 overexpression significantly inhibited cell proliferation, apoptosis and cell cycle. Additionally, luciferase reporter assay revealed that Gli3 may be a novel and direct target of miR-218 in CC. Taken together, the results of the present study suggest that miR-218 overexpression or Gli3 knockdown may have potential as therapeutic strategies for the treatment of CC.