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MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin

Authors Yin Z, Ren W

Received 7 June 2018

Accepted for publication 4 September 2018

Published 23 January 2019 Volume 2019:12 Pages 759—771

DOI https://doi.org/10.2147/OTT.S176618

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 4

Editor who approved publication: Dr Federico Perche


Zhaojun Yin, Weiru Ren

Gynaecology Ward of Maternal and Child Health Hospital, Shizhong District, Zaozhuang 277100, Shandong, People’s Republic of China

Background: MicroRNA-217 (miR-217) has been demonstrated to participate in the tumorigenesis and progression of various types of cancers. Nevertheless, the role of miR-217 in cervical carcinoma still remains not fully elucidated. This current work sought to investigate the role of miR-217 in the growth, migration, and invasion of cervical carcinoma and detect the role of miR-217 in the chemosensitivity of cervical carcinoma cell to cisplatin.
Materials and methods: The levels of miR-217 in 65 pairs of cervical carcinoma tissues and matched normal tissues were detected using quantitative real-time-PCR assay. The roles of miR-217 on the growth, apoptosis, migration, and invasion of cervical cancer SiHa and Ca-Ski cells were analyzed using Cell Counting Kit-8, flow cytometry, wound healing, and Transwell invasion assays, respectively. The target of miR-217 was identified using the online analysis tool TargetScan (http://www.targetscan.org/vert_72/) and was verified by luciferase reporter and immunoblotting assays. The xenograft tumor model was constructed to explore the impact of miR-217 on the growth of cervical carcinoma cell in vivo.
Results: The level of miR-217 was remarkably lower in cervical carcinoma tissues than that in noncancerous tissues. Overregulation of miR-217 markedly suppressed the aggressiveness of cervical cancer cell and induced cell apoptosis through regulating V-Ki-Ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS). Finally, upregulation of miR-217 enhanced the chemosensitivity of both SiHa and Ca-Ski cervical cancer cells toward cisplatin.
Conclusion: Altogether, upregulation of miR-217 inhibits the aggressiveness phenotypes of cervical carcinoma cell via regulating KRAS gene and increases the sensitivity of cervical cancer cell to cisplatin.

Keywords: cervical cancer, cisplatin, miR-217, KRAS

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