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Propofol Inhibits the Progression of Cervical Cancer by Regulating HOTAIR/miR-129-5p/RPL14 Axis

Authors Sun N, Zhang W, Liu J, Yang X, Chu Q

Received 1 September 2020

Accepted for publication 10 November 2020

Published 19 January 2021 Volume 2021:14 Pages 551—564

DOI https://doi.org/10.2147/OTT.S279942

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr William Cho


Nai Sun,* Wei Zhang,* Jiaying Liu, Xiaochen Yang, Qinjun Chu

Department of Anesthesiology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou City, Henan Province, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Qinjun Chu
Department of Anesthesiology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, No. 16 Tongbai North Road, Zhongyuan District, Zhengzhou 450007, Henan Province, People’s Republic of China
Tel/Fax +86 371-67690273
Email yxchen615@163.com

Background: Propofol has been proposed to function as a tumor suppressor in various human cancers. In this study, we aimed to investigate the anti-tumor effect of propofol on cervical cancer (CC).
Methods: Cell Counting Kit-8 (CCK-8) assay, colony formation assay, flow cytometry analysis, transwell assay and wound healing assay were conducted for cell viability, colony formation, apoptosis, invasion and migration, respectively. Western blot assay was used for protein levels. Quantitative real-time polymerase chain reaction (qRT-PCR) was used for HOX antisense intergenic RNA (HOTAIR), miR-129-5p and RPL14 levels. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were executed to verify the interaction between miR-129-5p and HOTAIR or RPL14. Murine xenograft model assay was used for the role of propofol in tumor progression in vivo.
Results: Propofol treatment suppressed CC cell viability, colony formation, invasion and migration and facilitated apoptosis. Propofol treatment led to a marked reduction in HOTAIR level in CC cells. HOTAIR overexpression promoted cell colony formation, invasion and migration and repressed apoptosis in CC cells and propofol-treated CC cells. For mechanism analysis, HOTAIR positively regulated RPL14 expression via acting as the sponge of miR-129-5p. MiR-129-5p overexpression reversed the impacts of HOTAIR on the malignant behaviors of propofol-treated CC cells. Furthermore, miR-129-5p inhibition accelerated the progression of CC cells, while RPL14 interference rescued the effect. In addition, propofol treatment restrained tumor growth of CC in vivo.
Conclusion: Propofol inhibited CC development by modulation of HOTAIR/miR-129-5p/RPL14 axis.

Keywords: propofol, cervical cancer, HOTAIR, miR-129-5p, RPL14

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