Long non‑coding RNA NEF inhibits proliferation and promotes apoptosis of laryngeal squamous cell carcinoma cells by inhibiting Wnt/β‑catenin signaling
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- Published online on: March 15, 2019 https://doi.org/10.3892/ol.2019.10150
- Pages: 4928-4934
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Copyright: © Cui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The present study aimed to investigate the involvement of the recently identified long non‑coding RNA neighboring enhancer of FOXA2 (lncRNA NEF) in laryngeal squamous cell carcinoma (LSCC). In this study, the expression levels of lncRNA NEF in tumor tissues and paired adjacent normal tissues were detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Serum levels of NEF in patients with LSCC and healthy controls were also measured using RT‑qPCR. Clinical and follow‑up data of patients with LSCC were retrospectively analyzed. Diagnostic and prognostic values of serum NEF were evaluated by receiver operating characteristic curve and survival curve analysis, respectively. In addition, a NEF expression vector was constructed and transfected into human LSCC cells. The effects of NEF overexpression on cell proliferation, apoptosis and β‑catenin expression were explored by Cell Counting kit‑8 cell proliferation assay, MTT assay and western blotting. NEF was significantly downregulated in tumor tissues compared with in paired adjacent normal tissues of patients with LSCC. Serum levels of NEF were significantly lower in patients with LSCC than in healthy controls. Low serum levels of NEF distinguished patients with LSCC from healthy controls, and also indicated shorter postoperative survival. NEF overexpression inhibited proliferation and promoted apoptosis of LSCC cells, and also downregulated β‑catenin expression. No significant effects of Wnt agonist on NEF expression were identified; however, Wnt agonist reduced the effects of NEF overexpression on cancer cell proliferation and apoptosis. In conclusion, lncRNA NEF may inhibit proliferation and promote apoptosis of LSCC cells by inhibiting Wnt/β‑catenin signaling.
