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Long Noncoding RNA FBXL19-AS1 Expedites Cell Growth, Migration and Invasion in Cervical Cancer by miR-193a-5p/PIN1 Signaling

Authors Wan S, Ni G, Ding J, Huang Y

Received 11 May 2020

Accepted for publication 27 August 2020

Published 7 October 2020 Volume 2020:12 Pages 9741—9752


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Harikrishna Nakshatri

Su Wan,1 Guantai Ni,1 Jin Ding,1 Yuansheng Huang2

1Department of Obstetrics and Gynecology, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241000, People’s Republic of China; 2Department of Orthopedics, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241000, People’s Republic of China

Correspondence: Yuansheng Huang
Department of Orthopedics, Yijishan Hospital of Wannan Medical College, No. 2 Zheshan West Road, Jinghu District, Wuhu, Anhui 241000, People’s Republic of China
Tel +86 0553-5739999
Fax +86 0553-5738279

Background: Cervical cancer is one of the most prevalent malignancies in gynecology with increasing incidence in recent years. Long noncoding RNAs (lncRNAs) have been reported to regulate human cancers including cervical cancer. F-box and leucine-rich repeat protein 19 antisense RNA 1 (FBXL19-AS1) have been unmasked to exert carcinogenic functions in several cancers except cervical cancer.
Aim: Present study hammered at investigating the function and mechanism of FBXL19-AS1 in cervical cancer.
Methods: RT-qPCR was utilized to test gene expression. EdU staining, colony formation, transwell, flow cytometry and TUNEL assays were applied for measuring the impact of FBXL19-AS1 on cervical cancer cell functions. Moreover, RIP, RNA pull-down and luciferase reporter assays were utilized for detecting the correlations among FBXL19-AS1, miR-193a-5p and PIN1 (peptidylprolyl cis/trans isomerase, NIMA-interacting 1).
Results: FBXL19-AS1 exhibited elevated expression in cervical cancer tissues and cells. Silencing FBXL19-AS1 repressed cell proliferation through arresting cell cycle and stimulating apoptosis, and losing FBXL19-AS1 also restrained cell migration and invasion. Also, we discovered FBXL19-AS1 as a miR-193a-5p sponge, while miR-193a-5p was a tumor inhibitor in cervical cancer. Further, PIN1 was proved as the miR-193a-5p target, and FBXL19-AS1 augmented PIN1 expression in cervical cancer via sequestering miR-193a-5p. Of note, PIN1 accelerated the progression of cervical cancer, and its upregulation counteracted the impacts of depleted FBXL19-AS1 on cervical cancer cell functions.
Conclusion: FBXL19-AS1 contributes to malignant phenotypes in cervical cancer by sponging miR-193a-5p and regulating PIN1.

Keywords: FBXL19-AS1, miR-193a-5p, PIN1, cervical cancer

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