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

Authors Ben W, Zhang G, Huang Y, Sun Y

Received 16 October 2019

Accepted for publication 8 January 2020

Published 29 April 2020 Volume 2020:12 Pages 2925—2935

DOI https://doi.org/10.2147/CMAR.S234897

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Seema Singh


Wei Ben, Guangmei Zhang, Yangang Huang, Yuhui Sun

Obstetrics and Gynecology Department, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People’s Republic of China

Correspondence: Wei Ben
Obstetrics and Gynecology Department, The First Affiliated Hospital of Harbin Medical University, No. 23, Youzheng Street, Nangang District, Harbin 150001, Heilongjiang Province, People’s Republic of China
Email weimubao9525151@126.com

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.

Keywords: cervical cancer, miR-27a-3p, FBXW7

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