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LncRNA SNHG16 Promotes the Progression of Laryngeal Squamous Cell Carcinoma by Mediating miR-877-5p/FOXP4 Axis

Authors Wang X, Liu L, Zhao W, Li Q, Wang G, Li H

Received 21 February 2020

Accepted for publication 26 April 2020

Published 22 May 2020 Volume 2020:13 Pages 4569—4579

DOI https://doi.org/10.2147/OTT.S250752

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Leo Jen-Liang Su


Xiaoli Wang,1 Liming Liu,2 Wenfei Zhao,3 Qingyan Li,4 Guangsheng Wang,5 Huahui Li6

1Department of Clinical Laboratory, Jinan City People’s Hospital, Jinan People’s Hospital Affiliated to Shandong First Medical University, Jinan 271199, People’s Republic of China; 2Department of Otorhinolaryngology, Juye County Hospital of TCM, Heze 274900, People’s Republic of China; 3Department of Comprehensive Oncology Therapy, Qingdao Central Hospital, Qingdao University, Qingdao 266043, People’s Republic of China; 4Department of Clinical Laboratory, The People’s Hospital of Zhangqiu Area, Jinan 250200, People’s Republic of China; 5Department of Neurology, The People’s Hospital of Zhangqiu Area, Jinan 250200, People’s Republic of China; 6Department of Clinical Laboratory, Qingdao Municipal Hospital, Qingdao 266071, People’s Republic of China

Correspondence: Huahui Li Email jigcgk24849@163.com

Objective: Laryngeal cancer is a common malignant tumor in the ENT, of which laryngeal squamous cell carcinoma (LSCC) accounts for more than 90% of laryngeal cancer. The purpose of this study is to investigate the regulatory mechanism of lncRNA SNHG16 in LSCC.
Materials and Methods: Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to measure mRNA expression. Cell Counting Kit (CCK-8), Transwell and luciferase reporter assays, flow cytometric analysis and Western blot analysis were used to investigate the function of lncRNA SNHG16 in LSCC.
Results: SNHG16 expression was increased in LSCC tissues and cells. The abnormal expression of SNHG16 was associated with clinical stage and lymph node metastasis in LSCC patients. In addition, knockdown of SNHG16 restrained cell proliferation, migration and invasion in LSCC. More importantly, SNHG16 acted as a competitive endogenous RNA in LSCC and regulated FOXP4 expression by making miR-877-5p sponge. Further, SNHG16 promoted LSCC progression by interacting with miR-877-5p and FOXP4.
Conclusion: LncRNA SNHG16 promotes the progression of LSCC by sponging miR-877-5p and upregulating FOXP4.

Keywords: SNHG16, laryngeal squamous cell carcinoma, miR-877-5p, FOXP4

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