摘要
目的探讨miR-155调控前列腺癌细胞核因子转录κB(NF-κB)通路的分子机制。方法前列腺癌DU145和PC-3细胞株经Anti-miRTM miR-155抑制剂(anti-miR-155)转染后(实验组),采用蛋白印迹法(Western blot)和逆转录聚合酶链反应(RT-PCR)分别检测转染后细胞中RelA和RelB蛋白及mRNA表达水平,同时检测NF-κB活性及细胞因子水平。以转染AntimiR^(TM)阴性对照的DU145和PC-3细胞株为对照组。结果与对照组相比,实验组细胞RelA、白细胞介素(IL-6)、白细胞介素(IL-21)表达水平,以及NF-κB活性显著降低(P<0.05),RelB表达水平比较差异无统计学意义(P>0.05)。结论降低人前列腺癌细胞NF-κB活性和RelA表达水平,可能是miR-155参与调控前列腺癌生物学行为的分子机制之一。
Objective To explore the effects of miR-155 on nuclear factor-κB(NF-κB)pathways in prostate cancer cells.Methods RelA and RelB expression were evaluated by Western blot and reverse transcription-polymerase chain reaction(RT-PCR),NF-κB activity and cytokines were also detected in DU145 and PC-3cells after transfection of Anti-miR^TM miR-155inhibitor(anti-miR-155).Cells transfected by Anti-miRTMnegative control were set as control group.Results Compared with control group,levels of RelA protein,interleukin-6(IL-6),interleukin-21(IL-21)and activity of NF-κB were lower(P〈0.05),and the difference of RelB level was not significant(P〉0.05).Conclusion miR-155 could regulate prostate cancer development by modulating NF-κB activity of DU145 and PC-3cells by enhancement of RelA expression.
出处
《检验医学与临床》
CAS
2016年第20期2845-2846,2849,共3页
Laboratory Medicine and Clinic
基金
陕西省科技厅科技攻关项目(2010JM4043)