Abstract
MicroRNAs (miRs) serve important roles in the development of various types of human cancer, including nasopharyngeal carcinoma (NPC). In the present study, the expression levels of miR-663b in NPC were investigated and its role and underlying mechanisms were examined. Reverse transcription-quantitative polymerase chain reaction was performed to assess miR-663b expression levels in NPC tissues and C666-1 cells. TargetScan was applied to predict the putative targets of miR-663b and the dual luciferase reporter assay was used to confirm the predictions. To investigate the role of miR-663b in NPC, the NPC C666-1 cell line was transfected with miR-663b mimics, miR-663b inhibitors or negative control. The Cell Counting kit-8 assay was performed for cell proliferation detection and western blot analysis was applied to determine the expression levels of epithelial mesenchymal transition (EMT)-associated proteins. Results indicated that when compared with the adjacent normal tissues and the normal nasopharyngeal epithelial cells, miR-663b expression levels were significantly upregulated in the NPC tissues and the NPC cells (P<0.01). Notably, SMAD7 is a target gene of miR-663b and may be inhibited by miR-663b. Results indicated that NPC cell proliferation was significantly promoted by miR-663b mimics and significantly inhibited by miR-663b inhibitors (P<0.05 and P<0.01). In addition, the results indicated that, when compared with the negative control group the expression levels of E-cadherin were significantly decreased, whereas the expression levels of N-cadherin, Vimentin and matrix metalloproteinase-9 were significantly increased in the cells of the miR-663b mimics group (P<0.05 and P<0.01). However, cells in the miR-663b inhibitors group exhibited the opposite effects. In conclusion, the results of the present study indicated that miR-663b functions as a tumor promoter in NPC via promoting NPC cell proliferation and EMT by directly targeting SMAD7.