ABSTRACT
OBJECTIVE: To examine the potential mechanisms implicating miR-200c and epithelial-mesenchymal transition (EMT) in oral squamous carcinoma (OSC). MATERIALS AND METHODS: 32 pairs of OSC tissue samples and matched para-carcinoma normal tissue from patients undergoing routine surgery in the Xuzhou Stomatological Hospital from 2014-2016. HOC313 cells were cultured and transfected with miR-200c mimics and scrambled mimics. Cell migration, invasion assays, Luciferase reporter assay, and Western blot assay were conducted. RESULTS: miR-200c was downregulated in OSC tissues compared with adjacent normal tissues (n=32). miR-200c knockdown in the human oral cancer cell line HOC313 significantly suppressed cell invasion and migration, indicating the ability to inhibit tumor progression. Luciferase reporter assay indicated that miR-200c directly bound to the 3'-untranslated regions (3'-UTR) of Zinc finger E-box-binding homeobox (ZEB1) directly. Moreover, miR-200c significantly inhibited HOC313 cell EMT via negatively regulating ZEB1 protein expression. CONCLUSIONS: MiR-200c plays a pivotal role in controlling OSC metastasis via inhibiting EMT, which provides potential therapeutic targets for OSC.
