摘要
目的:探讨小鼠大肠癌CT26株中聚(腺苷二磷酸核糖)水解酶[Poly(ADP-ribose)glycohydrolase,PARG]对细胞间粘附因子表达的影响及其可能的机制。方法:以慢病毒为载体对CT26细胞株中PARG基因进行RNA沉默干扰,并筛选出稳定表达株。Realtime-PCR法检测沉默效果。Western blot法检测CT26细胞PARG、PARP、NF-κB和Pi-AKT(473)I、CAM-1、P-selectin的蛋白表达。结果:实验组与对照组(包括阴性对照组、空载体对照组)相比,PARG、PARP、Pi-AKT(473)、NF-κBI、CAM-1、P-selectin表达经统计学分析差异均有统计学意义(P<0.05)。结论:在大肠癌细胞株中,抑制PARG可以通过调节与NF-κB有关通路,进一步调节ICAM-1、P-selectin等细胞粘附因子。提示PARG在肿瘤癌栓形成过程中可能具有重要作用。
Objective：To clarify the possible mechanism of how PARG and PARP are to regulate intercellular adhesion factor through relevant signal pathways.Methods：Lentivirus carried shRNA interfered with the expression of PARG and steadily silenced cell lines.Realtime-PCR was used for testing the strength of shRNAi and Western blot was used to test the expressions of PARG,PARP,NF-κB,and Pi-AKT（473）,and LY249002 was served as Pi-AKT inhibitor.Results：The expressions of PARG,PARP,and NF-κB,ICAM-1,P-selectin in shRNAi group were weaker than those in the control groups（blank control and transfected with empty vector control group）;whereas Pi-AKT increased in the shRNAi group（P〈0.05）.Conclusion：The results suggest that PARG gene silencing may regulate NF-κB related signaling pathway and the intercellular adhesion factors such as ICAM-1 and P-selectin,which are reduced.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2011年第6期641-645,共5页
Journal of Chongqing Medical University
基金
国家自然科学基金资助项目(编号:NSFC30870946)
关键词
PARG
慢病毒转染
AKT磷酸化
细胞粘附
poly（ADP-ribose）glycohydrolase
lentiviral transfection
AKT phosphorylation
cell adhesion
