miR-199a通过NF-κB通路抑制子宫内膜干细胞黏附和侵袭的机制研究

The effects and action mechanism of miR-199a on the adhesion and invasion of endometrial stem cells in vitro

目的探讨miR-199a对子宫内膜干细胞(endometrial stem cells,EnSCs)黏附和侵袭的影响及机制。方法通过miR-199a抑制剂或阴性对照抑制EnSCs miR-199a表达后观察IKKβ、IκB-α、pIκB-α、NF-κBp65的表达水平;分别用NF-κBp65特异性siRNA(si-p65)或siRNA-NC转染细胞后观察E-cadherin、MMP-9、MMP-2、TIMP-1的表达水平。结果与对照组比较,miR-199a抑制剂上调EnSCs的IKKβ、NF-κBp65和pIκB-α蛋白水平,差异有统计学意义(P<0.05);转染siRNA(si-p65)后,E-cadherin与TIMP-1的蛋白表达上调,而MMP-2与MMP-9的蛋白表达下调,差异有统计学意义(P<0.05)。结论miR-199a通过NF-κB通路抑制子宫内膜干细胞黏附和侵袭。

Objective To investigate the effects and action mechanism of miR-199a on the adhesion and invasion of endometrial stem cells(EnSCs)in vitro.Methods The expression levels of IKKβ,IκB-α,pIκB-αand NF-κBp65 were detected after treating EnSCs with miR-199a inhibitor or negative controls.The expression levels of E-cadherin,MMP-9,MMP-2 and TIMP-1 were detected after treating EnSCs with NF-κBp65 specific siRNA(si-p65)or siRNA-NC.Results As compared with those in control group,the expression levels of IKKβ,NF-κBp65 and pIκB-αproteins in EnSCs were up-regulated by miR-199a inhibitors(P<0.05).After transfection of siRNA(si-p65),the expression levels of E-Cadherin and TIMP-1 proteins were up-regulated,however,the expression levels of MMP-2 and MMP-9 proteins were down-regulated(P<0.05).Conclusion The miR-199a can inhibit the adhesion and invasion of endometrial stem cells through the NF-κB pathway.