Background
Maternally expressed 3 (MEG3), a long chain noncoding RNA (lncRNA), has verified its function as a suppressor in several kinds of cancers. However, the downstream mechanism of MEG3 in regulating the molecular mechanism of epithelial-mesenchymal transformation (EMT) in head and neck squamous cell carcinoma (HNSCC) progression demands further investigation.
Conclusions
This study indicated that the MEG3-miR-421-E-cadherin axis could be a new therapeutic target for HNSCC.
Methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression level of MEG3 in HNSCC and adjacent normal tissues of 51 cases. Luciferase report assay was used to detect the correlation between miR-421 and MEG3, and miR-421 and E-cadherin in HNSCC cell lines. Cell invasion and proliferation capacity were assessed through transwell and CCK8 assays. Scratch wound assay was used to assess cell migration capacity.
Results
Firstly, this study demonstrated that the expression of MEG3 was significantly downregulated in HNSCC compared to adjacent normal tissues. Overexpressed MEG3 inhibited cell proliferation, migration, and invasion in vitro. Secondly, MEG3 upregulated the expression of E-cadherin, which was instead downregulated by miR-421. MiR-421 was negatively regulated by MEG3 in HNSCC. Therefore, MEG3 regulated EMT by sponging miR-421 targeting E-cadherin in HNSCC. Conclusions: This study indicated that the MEG3-miR-421-E-cadherin axis could be a new therapeutic target for HNSCC.