siRNA阻断NF-κB通路抑制HepG2细胞增殖及NK杀伤抵抗性  

Blockade of NF-κB Signaling by SiRNA Arrested Growth of HepG2 Cells and Down-regulated Their Resistanceto NK Cell Mediated Cytotoxicity

作　　者：刘艳艳[1] 孙萍[1] 梁淑娟[1] 

机构地区：[1]潍坊医学院免疫学教研室山东省高校免疫学重点实验室,山东潍坊261053

出　　处：《潍坊医学院学报》2009年第1期24-25,41,共3页Acta Academiae Medicinae Weifang

基　　金：国家自然科学基金(30772497);山东省卫生高层次人才1020工程专项基金;教育部科学技术研究项目重点项目(205090);山东省科技攻关计划(2008GG10002007)

摘　　要：目的利用小干扰RNA(siRNA)阻断肝癌细胞HepG2中的NF-κB信号通路,研究其对肝癌细胞增殖活性及NK杀伤敏感性的影响。方法利用NF-κB p65 siRNA转染HepG2细胞,48h后分别进行Western blotting及ELISA检测NF-κB p65蛋白的表达;MTT法检测转染后细胞的增殖变化及对NK-92细胞杀伤敏感性的变化。结果转染NF-κB p65 siRNA后肝癌细胞中NF-κB p65蛋白表达的水平明显下降;MTT检测发现,与对照组相比,NF-κB p65 siRNA能够明显抑制HepG2细胞的增殖活性,同时使其对NK-92细胞介导的杀伤敏感性增加(P<0.05)。结论siRNA阻断NF-κB通路能够抑制肝癌细胞增殖及对NK细胞杀伤的抵抗性。Objective To analyze the effect of NF-κB p65 siRNA on growth capacity and sensitivity to NK cell mediated cytolysis of HepG2. Methods siRNA targeted against NF-κB p65 was transfected into HepG2 cells to block the aetviation of NF-κB signaling pathway. The expression level of NF-κB p65 was detected by Western blotting and ELISA. Cell viability and sensitivity to NK cell mediated cytolysis was detected by MTT. Results The expression level of NF-κB p65 protein in HepG2 cells was markedly decreased through transfection with NF-κB p65 siRNA. Proliferation of HepG2 cells transfeeted with NF-κB p65 siRNA was arrested while sensitivity of these cells to NK cell mediated cytotoxieity was significantly increased compared with HepG2 cells. Conclusion Blocking of NF-κB signaling pathway through p65 siRNA could abrogate proliferation of HepG2 cells and down-regulate their resistance to NK cell mediated cytotoxieity.

关 键 词：肝肿瘤 SIRNA NF-ΚB 增殖 

分 类 号：R392.12[医药卫生—免疫学]