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MiR-1193 Inhibits the Malignancy of Cervical Cancer Cells by Targeting Claudin 7 (CLDN7)

Authors Zhang B, Lin Y, Bao Q, Zheng Y, Lan L

Received 23 January 2020

Accepted for publication 2 May 2020

Published 19 May 2020 Volume 2020:13 Pages 4349—4358

DOI https://doi.org/10.2147/OTT.S247115

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Nicola Silvestris


Bin Zhang,* Yao Lin,* Qiufang Bao, Yantong Zheng, Lan Lan

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Fujian Medical University, Fujian 350005, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Bin Zhang Email zhangbin_fj787@126.com

Objective: MicroRNAs (miRNAs) are highly involved in cancer development, including in cervical cancer (CC). In this study, we aimed to investigate the role and possible mechanism of a poorly studied miRNA, miR-1193, in CC progression.
Materials and Methods: Expression of miR-1193 was determined in 60 pairs of cervical samples. The impacts of miR-1193 on CC cell proliferation, invasion and migration capacities were verified by CCK-8, transwell and wound healing assays, respectively. Then, bioinformatics prediction, luciferase reporter assay, qRT-PCR and Western blot were successively conducted to study the targeting of claudin 7 (CLDN7) by miR-1193. After CLDN7 was restored in miR-1193-overexpressed cells, the rescue effects were determined. Finally, CLDN7 expression was analyzed in cervical samples, and its expression correlation with miR-1193 was explored.
Results: Compared with paired normal tissues, miR-1193 was sharply decreased in abnormal tissues (intraepithelial lesions and cancerous tissues). Especially, miR-1193 expression was gradually decreased in low-grade squamous intraepithelial lesions, high-grade squamous intraepithelial lesions and CC. Enforced expression of miR-1193 inhibited CC cell proliferation, invasion and migration. Mechanistically, we confirmed CLDN7 as a target of miR-1193, and restoration of CLDN7 robustly rescued the tumor suppressing effects of miR-1193 in CC cells. CLDN7 was upregulated in abnormal cervical tissues and its expression exhibited inverse correlation with that of miR-1193 in CC.
Conclusion: Our results suggested that miR-1193 exerted tumor inhibitory roles in CC malignancy by directly targeting CLDN7.

Keywords: cervical cancer, miR-1193, tumor suppressing, CLDN7

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