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作 者:魏汝锐 张燕[2] 吴勤奋 苑杨[1] 阿不都拉·艾沙 Wei Rurui;Zhang Yan;Wu Qinfen;Yuan Yang;Abudoula Aisha(Department of Neurosurgery,the Second Affiliated Hospital of Xinjiang Medical University,Xinjiang Key Laboratory of Neurological Disorder Research,Urumqi 830054,China)
机构地区:[1]新疆医科大学第二附属医院神经外科,新疆神经系统疾病研究重点实验室,乌鲁木齐830054 [2]浙江中医药大学公共卫生学院
出 处:《脑与神经疾病杂志》2024年第11期716-721,共6页Journal of Brain and Nervous Diseases
基 金:新疆少数民族科技人才特殊培养计划科研项目(2020D03005)。
摘 要:目的分析极光激酶A(AURKA)对神经胶质瘤细胞增殖、迁移与侵袭的影响及其作用机制。方法sh-AURKA和sh-Con(阴性对照)转染U87细胞;细胞计数试剂盒(CCK-8)和细胞侵袭实验(Transwell)法分析、敲低AURKA对神经胶质瘤细胞增殖、迁移和侵袭能力的影响;蛋白印迹法检测敲低AURKA对神经胶质瘤细胞中丝切蛋白(Cofilin)相关蛋白表达的影响;将已转染sh-AURKA或sh-Con的U87细胞注射到BALB/c裸鼠颈部皮下,定期测量肿瘤体积,收集瘤体并称重。结果与sh-Con组比,sh-AURKA组的胶质瘤细胞增殖、迁移和侵袭能力显著降低(P<0.001);sh-AURKA组裸鼠体内的瘤体体积和瘤体质量明显降低(P<0.001),敲低AURKA后磷酸化Cofilin的表达明显升高。结论敲低AURKA能抑制胶质瘤细胞增殖、迁移和侵袭,其机制可能与增加Cofilin的磷酸化水平从而降低非磷酸化及AURKA的上皮间质转化机制有关。Objective To analyze the effect of aurora kinase A(AURKA)on proliferation,migration and invasion of glioma cells and its mechanism.Methods U87 cells were transfected with sh-AURKA and negative control(sh-Con);cell counting kit(CCK-8)and Transwell methods were used to analyze the effects of knockdown AURKA on the proliferation,migration and invasion of glioma cells;Western blot was used to detect the effect of knockdown AURKA on the expression of Cofilin related proteins in glioma cells;U87 cells transfected with sh-AURKA or sh-Con were injected subcutaneously into the neck of BALB/c nude mice.The tumor volume was measured regularly,and the tumor was collected and weighed.Results Compared with sh-Con group,the proliferation,migration and invasion of glioma cells in sh-AURKA group were significantly decreased(P<0.001);the tumor volume and mass in nude mice in sh-AURKA group decreased significantly(P<0.001),and the expression of phosphorylated Cofilin increased significantly after knockdown of AURKA.Conclusion Knocking down AURKA can inhibit the proliferation,migration and invasion of glioma cells,and its mechanism may be related to the mechanism of increasing the phosphorylation level of Cofilin and reducing the nonphosphorylation and the epithelial mesenchymal transformation of AURKA.
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