摘要
为了探讨miR-29b对人子宫内膜癌(endometrial cancer, EC) RL95-2细胞凋亡的影响及机制,本研究将RL95-2细胞转染miR-29b mimics和miR-NC后,采用MTT法检测细胞活力;运用Annexin V-PI法检测细胞凋亡;采用Western blotting检测Caspase-3蛋白表达;使用流式细胞术检测ROS水平。研究结果显示:与miR-NC组比较,miR-29b mimics过表达miR-29b组在培养24 h和48 h后的RL95-2细胞活力显著降低(p<0.05)。与miR-NC组比较,miR-29b mimics组的RL95-2细胞凋亡率显著增加(p<0.05)。与miR-NC组比较,miR-29b mimics组的RL95-2细胞Cleaved caspase-3蛋白表达水平显著增加(p<0.05)。此外,miR-29b mimics组的RL95-2细胞ROS水平明显低于miR-NC组(p<0.05)。本研究的初步结论表明:miR-29b可能通过调控ROS水平促进人RL95-2细胞凋亡。
To explore the role and the underlying mechanism of mi R-29 b on the apoptosis of human endometrial cancer(EC)RL95-2 cells,RL95-2 cells were transferred with miR-29 b mimics and miR-NC.Cell viability was detected using MTT assay.Cell apoptosis was determined by Annexin V-PI assay.The expression of caspase-3 protein was measured by Western blotting.ROS levels were detected by flow cytometry.After incubation for 24 h or 48 h,the cell viability in miR-29 b mimics group was obviously decreased when compared with miR-NC group(p<0.05).Besides,the cell apoptosis rate in miR-29 b mimics-treated RL95-2 cells was higher than that in miRNC group(p<0.05).Furthermore,the expression level of cleaved caspase-3 protein in the miR-29 b mimics group was markedly upregulated compared to the miR-NC group(p<0.05).We also observed that ROS levels in the miR-29 b mimics group were markedly lower than that in the mi R-NC group(p<0.05).miR-29 b promoted apoptosis of RL95-2 cells by regulating ROS.
作者
刘平
韩新彦
刘翠
乔雯岚
张易欣
Liu Ping;Han Xinyan;Liu Cui;Qiao Wenlan;Zhang Yixin(Handan Central Hospital,Handan,56000)
出处
《基因组学与应用生物学》
CAS
CSCD
北大核心
2019年第4期1944-1948,共5页
Genomics and Applied Biology
基金
邯郸市科学技术研究与发展计划项目(1623208079ZC)资助