摘要
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 study the impact and mechanism of DEK gene siRNA in human cervical cancer CaSki cell by observing of proliferation, cell cycle and apoptosis after DEK gene si lencing in human cervical cancer CaSki cell after DEK gene silencing. METHODS： The DEKsiRNA eukaryotic expression vector into CaSki cell,cell proliferation examined by MTT assay, cell cycle and cell apoptosis were analyzed by flow cytometry at 48h post DEK siRNA transfection. RESULTS： The growth inhibitin rate （53.2% ,P=0. 038） and apoptosis rate [（13.84±3.19）% ,P=0. 002）] of CaSki cells of psiRNA-hHDEK transfection increase significantly by comparing CaSki cells of non-transfected and psiRNA-hHlneo transfected; the cell number of G0/G1 phase in psiRNA-hHDEK transfection group （82. 65±5. 23） was higher than in controls （70.25±5.11） and in psiRNA-hHlneo transfec tion group （74. 36 ± 7. 49）, the difference was significant （P = 0. 003）; proliferation index of psiRNA-hHDEK transfected cell was 17. 35%, lower than non-transfected group 29. 75% and psiRNA-hHlneo transfection 25.64%, the difference was significant （P=0.02）. CONCLUSION： DEK gene silencing can inhibit reproduction and synthesis of DNA in tumor cells and inhibite cell proliferation and cell division,induce the apoptosis of CaSki cell.
出处
《中华肿瘤防治杂志》
CAS
2011年第10期758-761,共4页
Chinese Journal of Cancer Prevention and Treatment
基金
2008年辽宁省高等学校科研项目计划(2008862)
2009年中华医学科技奖叁等奖(200903124P0806)
