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作 者:刘渊渊 曾瑜[1] Liu Yuanyuan;Zeng Yu(Department of Neurosurgery,Xiangya Hospital,Central South University,Changsha 410008,China)
出 处:《中国医师杂志》2021年第12期1791-1794,共4页Journal of Chinese Physician
基 金:湖南省自然科学基金青年基金(2018JJ3809);中国博士后科学基金(2018M643006)。
摘 要:目的探讨AT丰富结合域1A(ARID1A)在胶质母细胞瘤侵袭中的作用及机制。方法体外培养人胶质瘤细胞U87,用Lipofectamin脂质体法将重组pCDNA3.1(+)-ARID1A转染至U87细胞为ARID1A过表达组,转染空质粒至U87细胞为vector组,未作处理的为空白对照组,qRT-PCR和Western blot验证其转染效率。采用Transwell侵袭实验检测细胞的侵袭能力;Western blot技术检测c-myc、MMP-2、MMP-9表达的变化。结果转染ARID1A真核表达质粒48 h后,ARID1A过表达组、vector组、空白对照组的细胞侵袭能力分别为(42.2±11.5)%、(98.6±4.8)%、(100.0±5.1)%,ARID1A过表达组与另外两组相比,差异有统计学意义(P<0.01);ARID1A过表达组c-myc、MMP-2、MMP-9蛋白的表达均低于vector组和空白对照组(P<0.01)。结论ARID1A可以通过抑制MMP-2/MMP-9表达来抑制胶质母细胞瘤的侵袭,可以作为潜在的胶质瘤治疗靶点。Objective To investigate the role and mechanism of AT-rich interactive domain 1A gene(ARID1A)in glioblastoma invasion.Methods Human glioblastoma cell line U87 was cultured in vitro.U87 cells transfected with recombinant pcDNA3.1(+)-ARID1A by lipofectamine liposome method as ARID1A overexpression group,and U87 cells transfected with empty plasmid as vector group.Untreated U87 cells were as blank control group.The transfection efficiency was verified by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR)and Western blot.Transwell invasion test was used to detect the invasion ability of cells,and Western blot was used to detect the protein expression of c-myc,matrix metalloproteinases(MMP)-2 and MMP-9.Results 48 hours after transfection with ARID1A eukaryotic expression plasmid,the cell invasion ability of ARID1A overexpression group,vector group and blank control group were(42.2±11.5)%,(98.6±4.8)%,(100.0±5.1)%.There was significant difference between ARID1A overexpression group and the other two groups(P<0.01);The expressions of c-myc,MMP-2 and MMP-9 in ARID1A overexpression group were lower than those in vector group and blank control group(P<0.01).Conclusions ARID1A can inhibit the invasion of glioblastoma by inhibiting the expression of MMP-2/MMP-9,and can be used as a potential therapeutic target for glioblastoma.
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