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作 者:李佳欣[1,2] 肖瑶[1] 李明亮 郑甜 刘丽波[1] LI Jia-xin;XIAO Yao;LI Ming-liang;ZHENG Tian;LIU Li-bo(Department of Neurobiology,College of Life Science,China Medical University,Shenyang 110122;106th Biological Sciences Specitalty,China Medical University,Shenyang 110004,China)
机构地区:[1]中国医科大学生命科学学院神经生物学教研室,辽宁沈阳110122 [2]中国医科大学,辽宁沈阳110004
出 处:《解剖科学进展》2024年第6期610-613,共4页Progress of Anatomical Sciences
基 金:国家自然科学基金(81402573);辽宁省自然科学基金(2019-MS-366,2021-MS-158)。
摘 要:目的研究Y-box结合蛋白2(YBX2)在脑胶质瘤微血管内皮细胞(GECs)中的表达,以及对GECs增殖、迁移和管形成的影响。方法培养人脑微血管内皮细胞(ECs)和GECs,应用Real-time PCR和Western blot方法检测YBX2的mRNA和蛋白表达;应用lipofectamine 3000将YBX2的沉默质粒转染人GECs,验证转染效率后,CCK8方法检测细胞活力;Transwell迁移实验检测细胞迁移能力;体外血管形成实验检测细胞的管形成能力;Real-time PCR和Western blot方法检测VEGFR2的mRNA和蛋白的表达。结果YBX2在GECs中高表达;YBX2敲减能够显著抑制GECs的细胞活力和细胞迁移能力,抑制GECs形成的管分支数量和管的长度;同时YBX2敲减显著降低了GECs中VEGFR2的mRNA和蛋白表达水平。结论YBX2敲减通过下调VEGFR2的表达抑制脑胶质瘤的血管新生。Objective To study the expression of Y-box binding protein 2(YBX2)in glioma microvascular endothelial cells(GECs)and its effect on the proliferation,migration and tube formation of GECs.Methods Human brain endothelial cells(ECs)and GECs were cultured,and the mRNA and protein expressions of YBX2 were detected by Real-time PCR and Western blot assays.The silencing plasmid of YBX2 was transfected into GECs by lipofectamine 3000.After verifying the transfection efficiency,the cell viability of GECs was detected by CCK8 assay,the migration ability of GECs was detected by Transwell migration assay,and the tube formation ability of GECs was detected by Matrigel tube formation assay.Meanwhile,the mRNA and protein expressions of VEGFR2 were detected by Real-time PCR and Western blot assays.Results YBX2 was highly expressed in GECs.Knockdown of YBX2 could significantly inhibit the cell viability and migration ability of GECs,and inhibit the number of tube branches and tube length formed by GECs.Meanwhile,Knockdown of YBX2 significantly decreased the mRNA and protein expression levels of VEGFR2 in GECs.Conclusion Knockdown of YBX2 inhibits the glioma angiogenesis by down-regulating the expression of VEGFR2.
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