[Circular RNA circHIPK3 acts as the sponge of microRNA-124 to promote human oral squamous cell carcinoma cells proliferation].

Objective: To explore the expression and clinical significance of circular RNA circHIPK3 in oral squamous cell carcinoma (OSCC), analyze the effect of circHIPK3 on the proliferation of OSCC cells. Methods: The expression of circHIPK3 in OSCC tissues, adjacent non-cancerous tissues and OSCC cell lines were detected by quantitative real-time polymerase chain reaction (qPCR). The correlations between the expression of circHIPK3 in OSCC tissues and the clinicopathological features were analyzed as well. circHIPK3-specific siRNA si-circHIPK3 and negative control siRNA si-NC were designed and synthesised and used to transfect CAL27 and SCC15 cells respectively. The proliferation capacity of CAL27 and SCC15 cells after transfection with si-circHIPK3 was detected by CCK-8 assay. The expression of miR-124 in OSCC was detected by qPCR, and the correlation between expression of circHIPK3 and the expression of miR-124 was analyzed. Using qPCR to detect the expression of miR-124 in CAL27 and SCC15 cells after transfection with si-circHIPK3 and si-NC respectively. Furthermore, using CCK-8 assay to detect the proliferation capacity of CAL27 and SCC15 cells after transfection with si-NC, si-circHIPK3, miR-124 mimic, si-circHIPK3+miR-124 inhibitor. Results: The expression of circHIPK3 in OSCC tissues [2.23 (1.86, 3.00)] was significantly higher than that of the adjacent non-cancerous tissues [1.05 (0.85, 1.26)] ( U =1 094, P= 0.000). The expression of circHIPK3 in CAL27 (3.02±0.51) and SCC15 cells (3.16±0.75) was higher than those of human normal oral keratinocytes (hNOK) (1.26±0.30) ( P= 0.000). The expression of circHIPK3 was found to be closely associated with TNM stage ( P< 0.05) and tumor grades ( P< 0.05). Knockdown of circHIPK3 can inhibit proliferation of CAL27 and SCC15 cells ( P< 0.05). The expression of miR-124 in OSCC tissues (0.61±0.35) was significantly lower than that in adjacent non-cancerous tissues (1.13+0.39) ( t= -5.36, P< 0.05). Correlation analysis showed that the expression of circHIPK3 in OSCC was negatively correlated with the expression of miR-124 ( r= -0.767, P< 0.001). Moreover, down-regulation of miR-124 rescued the phenotype induced by knockdown of circHIPK3. Conclusions: The expression of circHIPK3 in OSCC was increased, and silencing of circHIPK3 expression can inhibit the proliferation of OSCC cells. Our results suggest that circHIPK3 may play a key role in the occurrence and development process of OSCC through the regulation of miR-124 expression.