miR-106b induces the apoptosis and inhibits the proliferation of nasopharyngeal carcinoma cells / 西安交通大学学报(医学版)

ABSTRACT

Objective To investigate the effect of miR-106b on the apoptosis and proliferation of nasopharyngeal carcinoma (NPC ) cells. Methods We analyzed differences in miRNA expression in nasopharyngeal carcinoma and adjacent normal tissues with miRNA microarray.Taq Man miRNA detection kit and Real-time fluorescence quantitative PCR were used to detect the expressions of miR-106 and RhoC mRNA in nasopharyngeal carcinoma and adjacent tissues.The miR-106b and target gene binding sites were predicted with miRnada.The target gene was verified by double luciferase.Western blot was used to detect the expression of RhoC regulated by miR-106b.Annexin and TUNEL were used to detect the effect of miR-106b on the apoptosis of nasopharyngeal carcinoma cells;the effect of miR-106b on the proliferation of nasopharyngeal carcinoma cells was detected by MTT assay.Results miRNA microarray analysis showed that the expression of miR-106b was lower in NPC tissues than in adjacent normal tissues.The results of RT-PCR showed that the expression of miR-106b in nasopharyngeal carcinoma was decreased (P <0.05)while the expression of RhoC was increased in nasopharyngeal carcinoma (P <0.05).The expressions of miR-106b and RhoC in NPC were negatively correlated (r =-0.5866, P <0.001).The results of luciferase reporter assay showed that the activity of luciferase in miR-106b group was lower than that in empty plasmid group (P < 0.05 ).The results of Western blot showed that miR-106b could decrease the expression of RhoC in NPC tissues (P <0.05).Annexin V-PI and TUNEL showed that the apoptosis ofnasopharyngeal carcinoma cells was significantly higher in miR-106 group than in empty plasmid group (P <0.05). MTT results showed that the proliferation of nasopharyngeal carcinoma cells in miR-106b group was lower than that in empty plasmid group (P <0.05).Conclusion miR-106b may induce the apoptosis of nasopharyngeal carcinoma cells and inhibit the proliferation of nasopharyngeal carcinoma cells by down-regulating the expression of RhoC.