骨形态发生蛋白受体Ⅱ对肝癌细胞增殖与侵袭的影响  

Effect of Bone Morphogenetic Protein Receptor-Ⅱ on Proliferation and Invasion of Hepatocellular Carcinoma Cells

作　　者：冯鹏程 左为汉 吴建兵[1] FENG Peng-cheng;ZUO Wei-han;WU Jian-bing(Department of Oncology of the Second Affiliated Hospital of Nanchang Universit;Jiangxi Key Laboratory of Clinical and Translational Cancer Research,Nanchang 330006,Chin)

机构地区：[1]南昌大学第二附属医院肿瘤科江西省肿瘤临床转化研究重点实验室,南昌330006

出　　处：《南昌大学学报（医学版）》2018年第3期5-10,19,共7页Journal of Nanchang University：Medical Sciences

基　　金：江西省教育厅项目(GJJ14053)

摘　　要：目的探讨骨形态发生蛋白受体Ⅱ(bone morphogenetic protein receptorⅡ,BMPR-Ⅱ)对肝癌细胞增殖和侵袭能力的影响及其可能的机制。方法构建BMPR-Ⅱ过表达载体(overexpression-LV-BMPR-Ⅱ组)和BMPR-ⅡsiRNA干扰表达载体(LV-SH-BMPR-Ⅱ组),同时设立BMPR-Ⅱ过表达阴性对照组(overexpression-LV-CON组)与BMPR-ⅡsiRNA干扰表达阴性对照组(LV-SH-CON组),分别转染人肝癌Hep G2细胞,使用Real-time PCR和Western blot技术检测转染后的Hep G2细胞BMPR-ⅡmRNA与蛋白的相对表达量,采用CCK-8、Transwell实验检测4组Hep G2细胞的增殖和侵袭能力,通过Western blot检测PI3K/AKT/m-TOR信号通路相关蛋白的表达水平。结果 BMPR-ⅡmRNA和蛋白表达水平、Hep G2细胞的增殖和侵袭能力及p-PI3K、p-AKT、pm-TOR蛋白表达水平,overexpression-LV-BMPR-Ⅱ组较overexpression-LV-CON组均显著增加(P<0.05),LVSH-BMPR-Ⅱ组较LV-SH-CON组均显著减少(P<0.05)。结论 BMPR-Ⅱ通过上调PI3K/AKT/m-TOR信号通路促进肝癌HepG2细胞增殖和侵袭能力。ObjectiveTo investigate the effect of bone morphogenetic protein receptor-Ⅱ（BMPR-Ⅱ） on the proliferation and invasion of hepatocellular carcinoma cells and its possible mechanisms of action.Methods The vectors of BMPR-Ⅱ overexpression（overexpression-LV-BMPR-Ⅱ group）,BMPR-Ⅱ siRNA（LV-SH-BMPR-Ⅱ group）,negatively controlled BMPR-Ⅱ overexpression（overexpression-LV-CON） and negatively controlled BMPR-Ⅱ siRNA（LV-SH-CON group） were constructed and transfected into Hep G2 cells,respectively.The expression levels of BMPR-Ⅱ mRNA and protein were detected by real-time PCR and Western blot,respectively.The proliferation and invasion of Hep G2 cells were measured by CCK-8 and transwell assays.The expression of PI3K/AKT/m-TOR signaling pathway-related proteins was determined by Western blot.Results The expression of BMPR-Ⅱ mRNA and BMPR-Ⅱ,p-PI3K,p-AKT and p-m-TOR protein and the proliferation and invasion ability of Hep G2 cells in overexpression-LV-BMPR-Ⅱ group were higher than those in overexpression-LV-CON group（ P 〈0.05）,and those in LV-SH-BMPR-Ⅱ group were lower than those in LV-SH-CON group（ P 〈0.05）.Conclusion BMPR-Ⅱ promotes the proliferation and invasion of HepG2 cells through up-regulating PI3K/AKT/m-TOR signaling pathway.

关 键 词：骨形态发生蛋白受体Ⅱ 肝细胞癌 增殖 侵袭 

分 类 号：R735.7[医药卫生—肿瘤]