MiR-92a inhibits proliferation and promotes apoptosis of OSCC cells through Wnt/β-catenin signaling pathway

T.-L. Zheng, K. Cen

Department of Dental Surgery, Yantaishan Hospital, Yantai, China. cenkai1974@163.com

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• Oncology

OBJECTIVE: The aim of this study was to investigate the role of micro ribonucleic acid (miR)-92a in the pathogenesis of oral squamous cell carcinoma (OSCC).

MATERIALS AND METHODS: The relative expression level of miR-92a in OSCC cell lines and normal oral epithelial keratinocyte cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Subsequently, the effects of miR-92a silencing on proliferation and apoptosis of OSCC cells were determined via cell counting kit-8 (CCK-8) assay, flow cytometry, and colony formation assay, respectively. Whether miR-92a could bind to the 3’-untranslated region (3’-UTR) of target mRNA was detected using Dual-Luciferase reporter gene assay. Furthermore, changes in Wnt/β-catenin pathway-associated proteins were explored via Western blotting.

RESULTS: The expression of miR-92a in OSCC cell lines was significantly higher than that of normal oral epithelial keratinocyte cell lines (p<0.05). Silencing of miR-92a significantly inhibited proliferation and promoted apoptosis of OSCC cells (p<0.05). Luciferase reporter gene assay confirmed that miR-92a could bind to the 3’-UTR of Kruppel-like factor 4 (KLF4) gene. After miR-92a silencing, the expressions of Wnt/β-catenin pathway-associated proteins were remarkably down-regulated, including β-catenin, c-Myc, and Wnt3a (p<0.05).

CONCLUSIONS: Silencing of miR-92a inactivates the Wnt/β-catenin signaling pathway by targeting KLF4, thereby inhibiting proliferation and promoting apoptosis of OSCC cells. Our findings suggest that miR-92a may be a potential therapeutic target for OSCC patients.

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