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目的:通过观察DEK基因沉默后对CaSki细胞增殖、细胞周期及凋亡影响,探讨DEK原癌基因siRNA对宫颈癌细胞的影响和机制。方法:将DEK siRNA真核表达载体转入CaSki细胞,转染48 h后,采用MTT法检测细胞增殖、流式细胞仪检测细胞凋亡和细胞周期改变情况。结果:与对照组和未转染组相比,转染psiRNA-hHDEK组CaSki细胞增殖的抑制率和凋亡率均增高,分别为53.2%和(13.84±3.19)%,P值分别为0.038和0.002;psiRNA-hHDEK转染组G0/G1期细胞比率(82.65±5.23)较对照组(74.36±7.49)和未转染组(70.25±5.11)增多,差异有统计学意义,P=0.003;psiRNA-hH-DEK转染组细胞增殖指数(17.35%)明显低于未转染组(29.75%)和对照组细胞(25.64%),差异有统计学意义,P=0.02。结论:DEK基因抑制可能诱导CaSki细胞凋亡,并能影响肿瘤细胞内DNA的复制和合成,抑制细胞的正常分裂,从而抑制细胞增殖。
OBJECTIVE: To investigate the effect and mechanism of DEK proto-oncogene siRNA on cervical cancer cells by observing the effect of DEK gene silencing on the proliferation, cell cycle and apoptosis of CaSki cells. Methods: The eukaryotic expression vector DEK siRNA was transfected into CaSki cells. After 48 h of transfection, the cell proliferation was detected by MTT assay. The apoptosis and cell cycle changes were detected by flow cytometry. Results: Compared with the control group and the untransfected group, the proliferation and apoptosis rates of CaSki cells transfected with psiRNA-hHDEK were significantly higher (53.2% vs (13.84 ± 3.19)%, P = 0.038 and 0.002. The percentage of cells in G0 / G1 phase in psiRNA-hHDEK transfected group was significantly higher than that in control group (74.36 ± 7.49) and non-transfected group (70.25 ± 5.11) (82.65 ± 5.23, P = 0.003) The proliferation index (17.35%) in -hH-DEK transfected group was significantly lower than that in untransfected group (29.75%) and control group (25.64%), the difference was statistically significant (P = 0.02). CONCLUSION: DEK gene knockdown may induce apoptosis of CaSki cells and affect DNA replication and synthesis in tumor cells, inhibiting normal cell division and inhibiting cell proliferation.