lncRNA RASSF8‑AS1 suppresses the progression of laryngeal squamous cell carcinoma via targeting the miR‑664b‑3p/TLE1 axis

Liu,Tao; Meng,Wenxia; Cao,Huan; Chi,Weiwei; Zhao,Lei; Cui,Weina; Yin,Huan; Wang,Baoshan

doi:10.3892/or.2020.7771

lncRNA RASSF8‑AS1 suppresses the progression of laryngeal squamous cell carcinoma via targeting the miR‑664b‑3p/TLE1 axis

Authors:
- Tao Liu
- Wenxia Meng
- Huan Cao
- Weiwei Chi
- Lei Zhao
- Weina Cui
- Huan Yin
- Baoshan Wang
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Affiliations: Department of Otorhinolaryngology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, Department of Otorhinolaryngology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050031, P.R. China, Department of Otorhinolaryngology, The Affiliated Hospital of Hebei University, Baoding, Hebei 071000, P.R. China
Published online on: September 16, 2020 https://doi.org/10.3892/or.2020.7771
Pages: 2031-2044
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding (lnc)RNAs have been found to play a crucial role in tumor progression. The present study aimed to investigate the association between lncRNA RASSF8‑AS1 and laryngeal squamous cell carcinoma (LSCC) and the underlying mechanisms. Reverse transcription‑quantitative PCR was used to measure the mRNA expression level of RASSF8‑AS1, microRNA(miR)‑664b‑3p and transducin‑like enhancer of split 1 (TLE1) in LSCC. The associations between RASSF8‑AS1 and miR‑664b‑3p, and between miR‑664b‑3p and TLE1 were investigated using a dual luciferase reporter assay, while the former was further verified using an RNA immunoprecipitation (RIP) assay. The association between RASSF8‑AS1 and miR‑664b‑3p on cell biological functions was investigated in vitro using MTS, colony formation and Transwell assays. The RASSF8‑AS1 mRNA expression level was decreased in LSCC cell lines and carcinoma tissues, while overexpression of RASSF8‑AS1 reduced the migration, invasion and proliferation abilities of LSCC cells. Furthermore, luciferase and RIP assays confirmed that RASSF8‑AS1 was a competitive endogenous (ce)RNA by sponging miR‑664b‑3p to activate TLE1. miR‑664b‑3p was negatively modulated by RASSF8‑AS1; however, TLE1 was positively regulated by RASSF8‑AS1. Functionally, RASSF8‑AS1 acted as a ceRNA to upregulate TLE1 by sponging miR‑664b‑3p. In conclusion, the RASSF8‑AS1/miR‑664b‑3p/TLE1 axis acts by suppressing LSCC progression and may provide a novel insight for the molecular mechanism of LSCC.

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