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10.3892/etm.2017.4347

http://scihub22266oqcxt.onion/10.3892/etm.2017.4347
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C5450772!5450772!28588663
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suck abstract from ncbi


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pmid28588663      Exp+Ther+Med 2017 ; 13 (6): 2715-22
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  • MicroRNA-17-5p inhibits proliferation and triggers apoptosis in non-small cell lung cancer by targeting transforming growth factor ? receptor 2 #MMPMID28588663
  • Li H; Zhou H; Luo J; Huang J
  • Exp Ther Med 2017[Jun]; 13 (6): 2715-22 PMID28588663show ga
  • 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 ? receptor 2 (TGF?R2) 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 TGF?R2 in NSCLC cells. Furthermore, small interfering RNA-induced downregulation of TGF?R2 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 TGF?R2.
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