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作 者:甄洪涛 王朝亮[2] ZHEN Hongtao;WANG Chaoliang(Zhengzhou Central Hospital Affiliated to Zhengzhou University,Zhengzhou,450007)
机构地区:[1]郑州大学附属郑州中心医院,450007 [2]郑州大学第一附属医院,450000
出 处:《实用癌症杂志》2022年第8期1219-1223,1228,共6页The Practical Journal of Cancer
摘 要:目的探讨Oct4B1基因沉默通过蛋白激酶B/糖原合成酶激酶3β/β-连环素(AKT/GSK-3β/β-catenin)通路对膀胱癌细胞上皮间质转化(EMT)的影响。方法Oct4B1-shRNA质粒和阴性对照质粒转入T24细胞,为shRNA组、shRNA-NC组,转染后AKT激动剂处理,为shRNA+AKT激动剂组、shRNA-NC+AKT激动剂组。检测4组侵袭、迁移及E-cadherin、Vimentin、N-cadherin、p-AKT、p-GSK-3β及β-catenin蛋白表达。结果与shRNA组比较,shRNA+AKT激动剂组、shRNA-NC组、shRNA-NC+AKT激动剂组穿膜细胞数、迁移率、E-cadherin蛋白表达量较高(P<0.05),且shRNA+AKT激动剂组<shRNA-NC组<shRNA-NC+AKT激动剂组(P<0.05)。与shRNA组比较,shRNA+AKT激动剂组、shRNA-NC组、shRNA-NC+AKT激动剂组Vimentin、N-cadherin、p-AKT、p-GSK-3β、β-catenin蛋白表达量较低(P<0.05),且shRNA+AKT激动剂组>shRNA-NC组>shRNA-NC+AKT激动剂组(P<0.05)。结论沉默Oct4B1可抑制膀胱癌细胞侵袭、转移及EMT过程,其机制可能与AKT/GSK-3β/β-catenin有关。Objective To investigate the effect of Oct4B1 gene silencing on the epithelial-mesenchymal transition(EMT)of bladder cancer cells through the protein kinase B/glycogen synthase kinase 3β/β-catenin(AKT/GSK-3β/β-catenin)pathway.Methods Oct4B1-shRNA plasmid and negative control plasmid were transferred into T24 cells,named shRNA group,shRNA-NC group,AKT agonist treatment after transfection,named shRNA+AKT agonist group,shRNA-NC+AKT agonist group.The 4 groups of invasion,migration and E-cadherin,Vimentin,N-cadherin,p-AKT,p-GSK-3βandβ-catenin protein expression were detected.Results Compared with shRNA group,shRNA+AKT agonist group,shRNA-NC group,shRNA-NC+AKT agonist group had higher number of transmembrane cells,migration rate,and E-cadherin protein expression(P<0.05),and shRNA+AKT agonist group<shRNA-NC group<shRNA-NC+AKT agonist group(P<0.05).Compared with the shRNA group,the shRNA+AKT agonist group,shRNA-NC group,shRNA-NC+AKT agonist group Vimentin,N-cadherin,p-AKT,p-GSK-3β,β-catenin protein expression were lower(P<0.05),and shRNA+AKT agonist group>shRNA-NC group>shRNA-NC+AKT agonist group(P<0.05).Conclusion Silencing Oct4B1 can inhibit the invasion,metastasis and EMT process of bladder cancer cells.The mechanism may be related to AKT/GSK-3β/β-catenin.
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