RESUMO
The aim of this research was to assess the function of microribonucleic acid (miR)-195 in the apoptosis and proliferation of oral squamous cell carcinoma (OSCC) cells as well as its action mechanism. The downstream target protein of miR-195 was predicted using the biological software. A quantitative polymerase chain reaction (qPCR) was implemented to examine the changes in expressions of miR-195 and its target protein toll-like receptor 4 (TLR4) in OSCC cell lines (TSCCA, Tca8223, Tb3.1, and CAL-27) and normal adult human gingival fibroblasts (HGFs), and the relation between their expressions was assessed. The expressions of phosphorylated proteins in nuclear factor-κB (NF-κB) pathway were determined through western blotting. miR-195 was expressed at a noticeably lower level in four OSCC cells than in HGFs, and the lowest level appeared in CAL-27 cells. Compared with miR-195 control, the miR-195 mimic could obviously raise the expression of miR-195. In CAL-27 cells with high expression of miR-195, the proliferation was inhibited and the apoptosis was evidently enhanced. OSCC cells exhibited evidently reduced protein and mRNA expression of TLR4, and miR-195 expression was inversely associated with TLR4 expression. It was uncovered from the dual-luciferase reporter assay that cells with wild-type TLR4 had prominently weakened luciferase activity relative to cells with mutant-type TLR4, revealing that the direct target of miR-195 is TLR4. The NF-κB pathway was impeded in cells that lowly expressed TLR4. miR-195 blocks the NF-κB pathway via inhibiting the expression of TLR4 in OSCC cells, thereby exerting an antitumor effect.
