摘要
目的探讨Gli促进肺腺癌A549细胞上皮-间质转化(epithelial-mesenchymal transition,EMT)的分子学机制。方法 Western blot法观察GANT61、N-Shh、GANT61&N-Shh分别处理A549细胞后对Gli1、Gli2、pAKT、AKT、β-catenin和Vimentin蛋白表达的影响;侵袭实验观察GANT61、N-Shh、GANT61&N-Shh对肺腺癌细胞迁移侵袭能力的影响。结果 GANT61&N-Shh组Gli1蛋白、Gli2蛋白、p-AKT蛋白、Vimentin蛋白、β-catenin蛋白及穿膜细胞数低于DMSO组和N-Shh蛋白组、高于GANT61组,N-Shh蛋白组高于DMSO组和GANT61组,GANT61组低于DMSO组,差异均有统计学意义(P<0.01);AKT蛋白各组间差异无统计学意义(P>0.05)。结论Gli1和Gli2表达上调可能通过PI3K/AKT途径促进肺腺癌A549细胞上皮-间质转化能力并最终促进细胞侵袭转移。
Objective To explore the molecular mechanisms by which Gli transcription factor inhibitor regulates epithelial-mesenchymal transition(EMT)in Lung Adenocarcinoma.MethodsThe protein expression of Gli1,Gli2,p-AKT,AKT,Vimentin andβ-catenin were observed by Western blot assay with respective treatment of GANT61,N-Shh,GANT61&N-Shh.Transwell assay were performed to detect cell invasion ability.Results GANT61&N-Shh group was lower than DMSO group and N-Shh protein group in expression of Gli1,Gli2,p-AKT,Vimentin and the number of membrane cells,and was higher than GANT61 group in the above indicators.NShh protein group was higher than DMSO group and GANT61 group.GANT61 group was lower than DMSO group,the difference was significant(P<0.01).AKT protein expression showed no significant difference among difference groups(P>0.05).Conclusion Up-regulated expression of Gli1 and Gli2 may promote epithelial mesenchymal transition and eventually promote cell invasion and metastasis of lung adenocarcinoma A549 cells through PI3 K/AKT pathway.
出处
《河北医科大学学报》
CAS
2018年第1期24-28,共5页
Journal of Hebei Medical University
基金
河北省引进留学人员资助项目(CY201613)
关键词
肺肿瘤
上皮-间质转化
肿瘤转移
lung neoplasms
epithelial-mesenchymal transition
neoplasm metastasis
