Long non‑coding RNA‑neighboring enhancer of FOXA2 inhibits the migration and invasion of small cell lung carcinoma cells by downregulating transforming growth factor‑β1
Affiliations: Department of Respiratory Medicine, The First People's Hospital of Tianmen City, Tianmen, Hubei 431700, P.R. China, Clinical Laboratory, The First People's Hospital of Tianmen City, Tianmen, Hubei 431700, P.R. China
- Published online on: March 15, 2019 https://doi.org/10.3892/ol.2019.10152
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Long non‑coding RNA‑neighboring enhancer of FOXA2 (lncRNA‑NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. The present study aimed to investigate the role of lncRNA‑NEF in small cell lung carcinoma (SCLC). Expression levels of lncRNA‑NEF in the lung biopsy tissues and plasma samples from patients with SCLC and from healthy controls were detected using reverse transcription‑quantitative polymerase chain reaction. Receiver operating characteristic curve analysis was performed to evaluate the diagnostic value of lncRNA‑NEF as a marker of SCLC. The association between plasma levels of lncRNA‑NEF and the clinical data of patients was analyzed using the χ2 test. An lncRNA‑NEF expression vector was prepared and transfected into SCLC cells, and cellular migration and invasion were detected using Transwell migration and invasion assays, respectively. The expression of transforming growth factor β1 (TGF‑β1) was detected using western blotting. The results demonstrated that the expression level of lncRNA‑NEF was lower in patients with SCLC compared with that in healthy controls. The expression level of lncRNA‑NEF in the plasma was associated with distant tumor metastasis. lncRNA‑NEF overexpression inhibited SCLC cell migration and invasion, resulting in TGF‑β1 downregulation, while treatment with exogenous TGF‑β1 reduced the inhibitory effects of lncRNA‑NEF overexpression on migration and invasion. Therefore, it was concluded that lncRNA‑NEF inhibited the migration and invasion of SCLC cells, which was potentially associated with the downregulation of TGF‑β1.