MiR-106a inhibits oral squamous cell carcinoma progression by directly targeting MeCP2 and suppressing the Wnt/β-Catenin signaling pathway

• Published in: American journal of translational research 2018, Vol.10 (11), p.3542-3554
• Main Authors: Zhang, Nan, Wei, Zhu-Liang, Yin, Jing, Zhang, Lu, Wang, Jin, Jin, Zuo-Lin
• Format: Article
• Language: English
• Subjects: Original
• ISSN: 1943-8141; 1943-8141

MicroRNAs (miRNAs) play critical roles in the tumorigenesis and progression of oral squamous cell carcinoma (OSCC). MiR-106a* functions as a tumor suppressor miRNA in several cancers; however, its role in OSCC has not been elucidated. We investigated the role of miR-106a* in human OSCC and explored its relevant mechanisms. The expression of miR-106a* was significantly downregulated in OSCC tissues and cell lines. The overexpression of miR-106a* inhibited OSCC cell proliferation and the cell cycle G1-S transition, and induced apoptosis. In contrast, inhibition of miR-106a* promoted cell proliferation and G1-S transition and suppressed apoptosis. The expression of miR-106a* inversely correlated with methyl-CpG binding protein 2 (MeCP2) expression in OSCC tissues. Using a luciferase reporter assay, MeCP2 was determined to be a direct target of miR-106a*. Overexpression of miR-106a* decreased MeCP2 expression at both the mRNA and protein levels, while inhibition of miR-106a* increased MeCP2 expression. Importantly, overexpression of MeCP2 eliminated the effects of miR-106a* overexpression in OSCC cells and silencing of MeCP2 recapitulated the cellular and molecular effects observed with miR-106a* overexpression. MeCP2 may promote OSCC cell proliferation by activating the Wnt/β-Catenin signaling pathway. Taken together, our study demonstrated that miR-106a* inhibited OSCC cell proliferation by suppression of the Wnt/β-Catenin signaling pathway and induced apoptosis through regulation of Caspase 3/9 expression via targeting MeCP2. These findings suggest that miR-106a* acted as a tumor suppressor in the progression of OSCC and may be a potential new target for OSCC diagnosis and therapy.