Long non‑coding RNA NEAT1 promotes migration and invasion of oral squamous cell carcinoma cells by sponging microRNA‑365

Liu,Xiaohua; Shang,Wenzhi; Zheng,Fuju

doi:10.3892/etm.2018.6493

Long non‑coding RNA NEAT1 promotes migration and invasion of oral squamous cell carcinoma cells by sponging microRNA‑365

Authors:
- Xiaohua Liu
- Wenzhi Shang
- Fuju Zheng
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Affiliations: Department of Endodontics, Jinan Stomatological Hospital, Jinan, Shandong 250001, P.R. China
Published online on: July 20, 2018 https://doi.org/10.3892/etm.2018.6493
Pages: 2243-2250
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 RNA nuclear enriched abundant transcript 1 (NEAT1) has been demonstrated to serve key roles in numerous human cancer types, but its function in oral squamous cell carcinoma (OSCC) and underlying regulatory mechanism have not been evaluated. The present study demonstrated that expression of NEAT1 was significantly higher in OSCC tissue and cell lines compared with adjacent non‑tumour tissue and normal oral keratinocytes, respectively. Additionally, upregulation of NEAT1 was significantly associated with advanced clinical stage and shorter survival time in patients with OSCC. Bioinformatics analysis and luciferase reporter gene assay data confirmed the interaction between NEAT1 and miR‑365, and it was revealed that NEAT1 may downregulate microRNA (miR)‑365 expression in OSCC cells. Furthermore, inhibition of NEAT1 expression led to a significant reduction in OSCC cell migration and invasion, which was accompanied by reduced matrix metalloproteinase (MMP)‑2 and MMP9 protein expression. By contrast, inhibition of miR‑365 eliminated suppressive effects of NEAT1 knockdown on OSCC cell migration and invasion. miR‑365 was significantly downregulated in OSCC tissue and cell lines and an inverse correlation between miR‑365 and NEAT1 expression in OSCC tissue was observed. To conclude, the present study demonstrated that NEAT1 promoted migration and invasiveness of OSCC cells by sponging miR‑365. The current study suggests that NEAT1 may serve as a novel therapeutic target for the treatment of OSCC.

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