MiRNA-148b和miRNA-152通过KIT/AKT信号通路诱导人肾癌细胞凋亡  

MiRNA-148b and miRNA-152 induce apoptosis in human renal carcinoma cells via the KIT/AKT signalling pathway

作　　者：周文宾[1,2] 毕兴杰 孙立江[4] 

机构地区：[1]青岛大学外科学教研室,266071 [2]潍坊医学院校医院外科,261053 [3]潍坊市第五人民医院皮肤科,261061 [4]青岛大学附属医院泌尿外科,266003

出　　处：《免疫学杂志》2016年第11期947-952,共6页Immunological Journal

基　　金：山东省高等学校科技计划(J14LL55)

摘　　要：目的探讨mi R-148b和mi R-152对肾癌细胞增殖和凋亡的影响及相关机制。方法通过模拟mi R-148b和mi R-152的过表达,研究这2种mi RNAs对786-O和SN12-PM6肾癌细胞株的存活率和凋亡率的影响。采用Western blot观察mi R-148b和mi R-152通过KIT/AKT信号通路对肾癌的调节作用。结果与对照组织比较,在786-O和SN12-PM6株肾癌细胞中,mi R-148b和mi R-152的转染通过抑制KIT的表达及其磷酸化降低了细胞的存活率并且加速了细胞凋亡。mi RNA转染后,p-AKT、AKT和Bcl-2的表达减少,而对p-m TOR、m TOR和Bcl-2L11表达的影响轻微。结论在786-O和SN12-PM6株肾癌细胞中,mi R-148b及mi R-152可通过KIT/AKT信号通路诱导细胞凋亡,这种作用与肿瘤的免疫反应相关。MicroRNAs（miRNAs） are involved in the regulation of immunity,including innate immunity and adaptive immunity.It is rarely reported that the expressions of microRNA-148b（miR-148b） and microRNA-152（miR-152） effect on renal cell carcinoma（RCC） cells and its antitumor mechanism,thus to investigate the effects and its relevant mechanism,we imitate the over expression of miR-148 b and miR-152 and detect the change of viability and apoptosis in two different RCC cell lines（786-0 and SN12-PM6）.The modulation effects of miR-148 b and miR-152 via the KIT/AKT pathways was determined by Western blotting.In RCC cell lines,we found that transient transfection of miR-148 b and miR-152 reduced viability and induced apoptosis by inhibiting of KIT expression and its phosphorylation,as compared to control tissue.p-AKT,AKT and Bcl-2 expression was reduced after miRNA transfection,whereas only slight influence on p-mTOR,mTOR and Bcl-2L11 was detected.In conclusion,miR-148 b and miR-152 can induce apoptosis in 786-0 and SN12-PM6 RCC cell lines by KIT/AKT signaling pathway,which is related to the immune response of the tumor.

关 键 词：MiR-148b miR-152 肾细胞癌 肿瘤免疫 凋亡 

分 类 号：R737.11[医药卫生—肿瘤]