MicroRNA-17-5p inhibits proliferation and triggers apoptosis in non‑small cell lung cancer by targeting transforming growth factor β receptor 2
- Hui Li
- Hui Zhou
- Jiashun Luo
- Jun Huang
Affiliations: Institute of Medical Examination, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China, Department of Medical Oncology, Tumor Hospital of Hunan Province, Changsha, Hunan 410000, P.R. China, Institute of Medical Research, Medical School of Jishou University, Jishou, Hunan 416000, P.R. China, Department of Orthopaedics, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China
- Published online on: April 18, 2017 https://doi.org/10.3892/etm.2017.4347
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MicroRNAs (miRs) are small non‑coding RNAs that suppress gene expression by directly binding to the 3'-untranslated region of their target mRNAs. Specific miRs serve key roles in the development and progression of non‑small cell lung cancer (NSCLC). The aim of the present study was to determine the mechanism of miR‑17‑5p in the regulation of NSCLC cell survival and proliferation. Reverse transcription‑quantitative polymerase chain reaction data indicated that miR‑17‑5p was significantly downregulated in 28 NSCLC tissues compared with 7 non‑tumorous lung tissues. Furthermore, lower miR‑17‑5p expression was associated with a higher pathological stage in NSCLC patients. Lower miR‑17‑5p expression was also observed in several common NSCLC cell lines, including SK‑MES‑1, A549, SPCA‑1, H460, H1229 and HCC827, compared with the bronchial epithelium cell line, BEAS‑2B. Additionally, overexpression of miR‑17‑5p significantly inhibited proliferation while inducing the apoptosis of NSCLC H460 cells. Subsequently, transforming growth factor β receptor 2 (TGFβR2) was identified as a direct target of miR‑17‑5p using a luciferase reporter assay. Western blot analysis confirmed that miR-17-5p negatively mediated the expression of TGFβR2 in NSCLC cells. Furthermore, small interfering RNA‑induced downregulation of TGFβR2 also suppressed the proliferation of H460 cells while triggering apoptosis. Therefore, the results of the current study suggest that miR‑17‑5p may inhibit proliferation and trigger apoptosis in NSCLC H460 cells at least partially by targeting TGFβR2.