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10.3892/etm.2017.4733

http://scihub22266oqcxt.onion/10.3892/etm.2017.4733
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C5609183!5609183!28962111
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suck abstract from ncbi


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pmid28962111      Exp+Ther+Med 2017 ; 14 (3): 1967-74
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  • MicroRNA-138 suppresses cell proliferation in laryngeal squamous cell carcinoma via inhibiting EZH2 and PI3K/AKT signaling #MMPMID28962111
  • Si F; Sun J; Wang C
  • Exp Ther Med 2017[Sep]; 14 (3): 1967-74 PMID28962111show ga
  • MicroRNA (miR)-138 generally has a suppressive role in various human cancer types; however, its role and the underlying mechanisms in laryngeal squamous cell carcinoma (LSCC) have remained to be elucidated. The present study assessed the clinical significance and regulatory mechanisms of miR-138 in LSCC progression. Reverse-transcription quantitative polymerase chain reaction analysis indicated that miR-138 was significantly downregulated in LSCC tissues and cell lines. In addition, the decreased expression of miR-138 was significantly associated with poor differentiation, lymph node metastasis and advanced clinical stage of LSCC. Restoration of miR-138 expression caused a significant decrease in the proliferation of Hep-2 LSCC cells, while knockdown of miR-138 significantly promoted Hep-2 cell proliferation. A luciferase reporter assay further identified enhancer of zeste homologue 2 (EZH2) as a direct target gene of miR-138, and the protein expression of EZH2 was negatively regulated by miR-138 in Hep-2 cells. Furthermore, overexpression of EZH2 eliminated the suppressive effects of miR-138 on Hep-2 cell proliferation via activation of phosphoinositide-3 kinase (PI3K)/AKT signaling. In addition, EZH2 was found to be significantly upregulated in LSCC tissues and to be inversely correlated to the miR-138 levels. The results of the present study demonstrated that miR-138 inhibits the proliferation of LSCC cells, at least partly via targeting EZH2 and inhibiting PI3 K/AKT signaling. The present study highlighted the clinical significance of the miR-138/EZH2 axis in LSCC.
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