Mol Med Rep
2018 Feb;17(2):2964-2972.
doi: 10.3892/mmr.2017.8227. Epub 2017 Dec 8.
miR‑96 inhibits EMT by targeting AEG‑1 in glioblastoma cancer cells
Shiyu Feng 1, Jie Yao 2, Zhibin Zhang 1, Yanyang Zhang 1, Zhiyuan Zhang 1, Jialin Liu 1, Wenlong Tan 2, Caihong Sun 1, Ling Chen 1, Xinguang Yu 1
Affiliations expand
PMID: 29257267
PMCID: PMC5783515
DOI: 10.3892/mmr.2017.8227
Abstract
The induction of epithelial to mesenchymal transition (EMT) is important for carcinogenesis and cancer progression. Previous studies have estimated that microRNA (miRNA/miR) expression is associated with EMT via the regulation of the expression of target genes. miR‑96 has been reported to exhibit a correlation with the EMT process. However, the functional role of miR‑96 and its mechanism in glioblastoma multiforme (GBM) remains to be completely elucidated. The objective of the present study was to investigate the functional role and mechanism of miR‑96 in the migration and invasion, in addition to proliferation, apoptosis and cell cycle distribution, of GBM. In the present study, the results suggested that the introduction of miR‑96 significantly inhibited the migration and invasion, in addition to proliferation and cell cycle progression, of GBM cells and promoted their apoptosis in vitro, leading to the hypothesis that miR‑96 may be a potential tumor suppressor. It was subsequently confirmed that astrocyte elevated gene‑1 (AEG‑1) was a direct target gene of miR‑96, using a luciferase assay and reverse transcription‑quantitative polymerase chain reaction analysis, in addition to western blotting. miR‑96 was observed to downregulate the expression of AEG‑1 at the mRNA and protein levels. Notably, AEG‑1 may suppress EMT by increasing the expression levels of E‑cadherin, an epithelial marker, and decreasing the expression levels of vimentin, a mesenchymal marker. Therefore, it was concluded that miR‑96 may impede the EMT process by downregulating AEG‑1 in GBM. Additionally, it was observed that inhibition of AEG‑1 led to a similar effect compared with overexpression of miR‑96 in GBM. In conclusion, the results of the present study demonstrated that miR‑96 may act as a tumor suppressor by regulating EMT via targeting of AEG‑1, suggesting that miR‑96 may be a potential biomarker and anticancer therapeutic target for GBM in the future.
参考链接：https://pubpeer.com/publications/F42B3B4D3D082CFF754EF1E68E7D43
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