MicroRNA‑138 suppresses cell proliferation in laryngeal squamous cell carcinoma via inhibiting EZH2 and PI3K/AKT signaling
- Fengzhi Si
- Jie Sun
- Chunli Wang
Affiliations: Department of Otorhinolaryngology, The Second Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830063, P.R. China
- Published online on: July 9, 2017 https://doi.org/10.3892/etm.2017.4733
Copyright: © Si
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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.