Abstract:Objective:To investigate the effect of siRNA (small interference RNA) silencing Gankyrin on the behavior of human laryngeal carcinoma cell lines Hep-2. Methods:The expression of mRNA and protein levels of Gankyrin was detected by using qRT-PCR and Western blot before and after transfection,respectively. The cell proliferation was measured by CCK-8 assay. The apoptosis rate and cell cycle of Hep-2 cells were determined by flow cytometry. Cell migration was detected by wound healing assay and transwell assay. Matrigel assay was performed to observe cell invasive ability. The expression of p53 protein after down-regulation of Gankyrin was detected by Western blot. Results:Compared with the negative control group and the blank control group,the expressions of Gankyrin mRNA and protein were downregulated in the Gankyrin siRNA group,and the differences were statistically significant (P < 0.001). CCK-8 assay showed that the proliferation rate of the Gankyrin siRNA group was significantly decreased (P < 0.001). Flow cytometry showed that the apoptosis rate of the Gankyrin siRNA group[(7.70 ± 1.12)%]was significantly higher than that in the negative control group[(2.34 ± 0.32)%]and the blank control group[(1.82 ± 0.29)%],and the differences were statistically significant (P < 0.001). Compared with the two controls,G1 phase cells of the Gankyrin siRNA group were significantly increased,S phase cells were significantly decreased,and the difference was statistically significant (P < 0.001). Wound healing assay and transwell assay showed that the cell migration ability in the Gankyrin siRNA group was decreased significantly (P < 0.01). Matrigel assay showed that Gankyrin siRNA did not impact the invasive ability of Hep-2 cell (P > 0.05). The expression of p53 protein in the Gankyrin siRNA group was increased (P < 0.001). Conclusion:Down-regulation of Gankyrin inhibited the proliferation and migration ability of Hep-2 cell,which may be associated with the alteration of apoptosis,cell cycle and the expression level of p53.