MicroRNA-17-5p inhibits proliferation and triggers apoptosis in non-small cell lung cancer by targeting transforming growth factor β receptor 2.

Abstract

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.