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作 者:杨建权 王国兵 张钶 戴永建 王志涛 阿尔帕提·买买提[1] 关玉华[3] 杨晓玲[3] 王增亮[1] Yang Jianquan;Wang Guobing;Zhang Ke(Department of Neurosurgery,The First Affiliated Hospital of Xinjiang Medical University,Urumqi,Xinjiang,830054,China)
机构地区:[1]新疆医科大学第一附属医院神经外科,新疆乌鲁木齐830054 [2]湖北医药学院附属人民医院神经外科,湖北十堰442000 [3]巴音郭楞蒙古自治州人民医院,新疆库尔勒841000
出 处:《黑龙江医学》2024年第23期2848-2850,共3页Heilongjiang Medical Journal
基 金:新疆维吾尔自治区自然科学基金项目(2021D01A02)。
摘 要:目的:探讨解整合素金属蛋白酶8(ADAM8)的N-糖基化对肿瘤生长和上皮间质转化(EMT)的影响。方法:通过定点突变技术将ADAM8的N-糖基化位点N436突变(N436Q)为谷氨酰胺,并在稳定转染的U87细胞中表达这一突变体。将这些细胞植入BALB/c裸鼠中,评估肿瘤生长情况。结果:ADAM8的N-糖基化缺陷突变体抑制了肿瘤的生长、减小了肿瘤体积和重量。进一步分析发现,ADAM8的N-糖基化缺陷突变体下调了EMT相关蛋白Vimentin和Claudin-1的表达并上调了E-cadherin的表达。结论:抑制ADAM8的N-糖基化可抑制小鼠胶质瘤的生长和EMT过程。Objective:To investigate the effects of N-glycosylation of A Disintegrin and Metalloproteinase 8(ADAM8)on tumor growth and epithelial mesenchymal transformation(EMT).Methods:The N-glycosylation site N436Q of ADAM8 was mutated to glutamine with site-specific mutation technique,and the mutant was expressed in stably transfected U87 cells.These cells were implanted in BALB/c nude mice,and tumor growth was assessed.Results:ADAM8 N-glycosylation defect mutant inhibited tumor growth and reduced tumor volume and weight.Further analysis showed that ADAM8 N-glycosylation deficient mutant down-regulated the expression of EMT-related proteins Vimentin and Claudin-1,and up-regulated the expression of E-cadherin.Conclusion:Inhibition of ADAM8 N-glycosylation can inhibit the growth of glioblastoma in mice by inhibiting EMT process.
关 键 词:解整合素金属蛋白酶8 N-糖基化 上皮间质转化 胶质母细胞瘤
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