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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Exp+Ther+Med
2017 ; 14
(3
): 1967-1974
Nephropedia Template TP
gab.com Text
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English Wikipedia
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
): 1967-1974
PMID28962111
show 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.