lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Yu,Lijiang; Huo,Lingli; Shao,Xiaolin; Zhao,Jizhi

doi:10.3892/ol.2020.12173

lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Authors:
- Lijiang Yu
- Lingli Huo
- Xiaolin Shao
- Jizhi Zhao
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Affiliations: Department of Oral and Maxillofacial Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, P.R. China, Department of Stomatology, Traditional Chinese Medicine Hospital of Shijingshan District, Beijing 100043, P.R. China, Department of Stomatology, Beijing Ditan Hospital, Capital Medical University, Beijing 100013, P.R. China
Published online on: September 30, 2020 https://doi.org/10.3892/ol.2020.12173
Article Number: 310
Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Recently, previous studies have shown that long non‑coding RNA (lncRNA) can act as a tumor promoter or inhibitor in the pathogenesis of oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of lncRNA SNHG5 is unknown in OSCC. Therefore, the functional mechanism of lncRNA SNHG5 in OSCC was initially revealed in this study. Here, RT‑qPCR and western blot analysis were used to assess mRNA and protein expression. The functional mechanism of SNHG5 was investigated by MTT, Transwell and luciferase reporter assays. The results showed that SNHG5 expression was upregulated in OSCC and promoted the viability, migration and invasion of OSCC cells. In addition, SNHG5 is the sponge of miR‑655‑3p in OSCC. And miR‑655‑3p was found to play an inhibitory effect in OSCC by interacting with SNHG5. Moreover, miR‑655‑3p directly targets FZD4 and negatively regulates its expression in OSCC. Functionally, FZD4 promoted the progression of OSCC by interacting with the SNHG5/miR‑655‑3p axis. In conclusion, lncRNA SNHG5 promotes cell proliferation, migration and invasion in OSCC by regulating miR‑655‑3p/FZD4 axis.

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