miR-361-3p调节恶性胶质瘤细胞功能的研究  

Studies of miR-361-3p in regulating the function of glioblastoma cells

作　　者：郭小叶[1] 冒平[1] 王佳[1] 廉海平[1] 王伟[1] 白晓斌[1] 宋锦宁[1] GUO Xiaoye;MAO Ping;WANG Jia;LIAN Haiping;WANG Wei;BAI Xiaobin;SONG Jinning(Department of Neurosurgery,the First Affiliated Hospital of Xi'an Jiaotong University,Shaanxi Province,Xi'an 710061,China)

机构地区：[1]西安交通大学第一附属医院神经外科

出　　处：《中国医药导报》2019年第28期7-11,共5页China Medical Herald

基　　金：国家自然科学基金青年项目（81602207、81802502）;陕西省自然科学基础研究计划项目（2018JM7062）

摘　　要：目的研究miR-361-3p在恶性胶质瘤(GB)细胞中的功能。方法培养LN299和U87MG细胞及人正常星形胶质细胞(NHA)。miR-361-3p的mimic或inhibitor及MTCP1的siRNA(si-MTCP1)转染U87MG细胞。RT-PCR和Western blot检测目标基因水平的变化。CCK-8和Caspase3试剂盒分别检测细胞的增殖和凋亡。荧光素酶基因报告实验检测miR-361-3p和MTCP1基因的结合。结果与NHA比较,miR-361-3p在LN299和U87MG中低表达。U87MG转染mimic可抑制MTCP1的表达和细胞增殖率,升高Caspase3活性,并减少WT-MTCP1的荧光素酶活性。U87MG转染inhibitor增加细胞增殖率,而转染si-MTCP1后细胞凋亡增加。结论miR-361-3p可能通过抑制MTCP1来抑制GB细胞的增殖并促进凋亡。Objective To study the role of miR-361-3p in glioblastoma(GB)cells.Methods LN299,U87MG and normal human astrocytes(NHA)were cultured.miR-361-3p mimic or inhibitor and MTCP1 siRNA(si-MTCP1)were transfected into U87MG cells,respectively.Gene expression was tested by RT-PCR and Western blot.Cell proliferation and apoptosis were measured by CCK-8 and Caspase3 kits,respectively.The binding of miR-361-3p and MTCP1 were detected by luciferase reporter assay.Results Relative to NHA,miR-361-3p levels were lower in LN299 and U87MG.Transfected with mimic,MTCP1 levels and the proliferation of U87MG cells were decreased,and the Caspase3 activity was increased,and luciferase activity in WT-MTCP1 was decreased.Furthermore,transfected with inhibitor,the proliferation of U87MG cells were increased,while the apoptosis rate in the si-MTCP1 group was increased.Conclusion MiR-361-3p may inhibit the proliferation and promote apoptosis of GB cells by inhibiting MTCP1.

关 键 词：恶性胶质瘤 细胞增殖 凋亡 miR-361-3p 

分 类 号：R739.41[医药卫生—肿瘤]