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MiR-27a-3p Regulated the Aggressive Phenotypes of Cervical Cancer by Targeting FBXW7

BACKGROUND: Abnormally expressed microRNAs (miRNAs) contribute greatly to the initiation and development of human cancers, including cervical cancer, by regulating the target mRNAs. MiR-27a-3p was up-regulated and acted as an oncogene in multiple cancers. However, the function of miR-27a-3p in cervi...

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Detalles Bibliográficos
Autores principales: Ben, Wei, Zhang, Guangmei, Huang, Yangang, Sun, Yuhui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7198449/
https://www.ncbi.nlm.nih.gov/pubmed/32431539
http://dx.doi.org/10.2147/CMAR.S234897
Descripción
Sumario:BACKGROUND: Abnormally expressed microRNAs (miRNAs) contribute greatly to the initiation and development of human cancers, including cervical cancer, by regulating the target mRNAs. MiR-27a-3p was up-regulated and acted as an oncogene in multiple cancers. However, the function of miR-27a-3p in cervical cancer has not been fully understood. METHODS: The expression of miR-27a-3p in cervical cancer tissues and cell lines was detected by RT-pPCR. MTT assay, colony formation assay and flow cytometry analysis were performed to determine the effects of miR-27a-3p on the growth of cervical cancer cells. The targets of miR-27a-3p were predicted using the miRDB database. Luciferase reporter assay was utilized to confirm the binding between miR-27a-3p and the 3ʹ-untranslated region (UTR) of targets. The expression of target proteins was determined by RT-qPCR and Western blot. RESULTS: Our results found that miR-27a-3p was overexpressed in cervical cancer tissues and cell lines. Down-regulation of miR-27a-3p significantly inhibited the proliferation, colony formation and promoted apoptosis of cervical cancer cells. Overexpression of miR-27a-3p enhanced the cell proliferation. miR-27a-3p was found to bind the 3ʹ-UTR of F-box and WD repeat domain containing 7 (FBXW7) and resulted in the down-regulation of FBXW7. The up-regulated level of miR-27a-3p was inversely correlated with that of FBXW7 in cervical cancer tissues. Additionally, reintroducing of FBXW7 significantly attenuated the promoting effect of miR-27a-3p on the proliferation of cervical cancer cells. CONCLUSION: These results indicated the growth-promoting function of miR-27a-3p in cervical cancer via targeting FBXW7. Our finding suggested the potential application of miR-27a-3p/FBXW7 axis in the diagnosis and treatment of cervical cancer.