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作 者:郭曼岚 刘蔚雯 勾梦壮 刘亚伟[2] 陈腾祥 GUO Manlan;LIU Weiwen;GOU Mengzhuang;LIU Yawei;CHEN Tengxiang(Key Laboratory of Stem Cell of Guizhou Province,Department of Physiology,Basic Medical College,Guizhou Medical University,Guiyang,550009,China;First College of Clinical Medicine;Laboratory for Precision Neurosurgery,Nanfang hospital,Southern MedicalUniversity,Guangzhou 510515,China)
机构地区:[1]贵州医科大学基础医学院生理学教研室//贵州省干细胞重点实验室,贵州贵阳550009 [2]南方医科大学南方医院神经外科//精准神经外科实验室,广东广州510515 [3]南方医科大学第一临床医学院,广东广州510515
出 处:《分子影像学杂志》2018年第4期483-487,共5页Journal of Molecular Imaging
基 金:国家自然科学基金(81472315);广东省自然科学基金(2017A030313497)
摘 要:目的研究药物康普瑞汀磷酸钠(CA4P)对人胶质瘤细胞U87细胞增殖迁移的影响以及相关信号通路。方法体外培养U87细胞并用不同浓度的CA4P处理,CCK8方法检测不同药物浓度对细胞活性的影响,划痕和transwell实验检测不同药物浓度对U87细胞迁移能力的影响,Western blot检测不同浓度处理后U87细胞中E-Cadherin蛋白。Path Scan对相关激活的通路进行检测。结果 CA4P能够明显抑制体外U87细胞增殖。划痕和transwell实验表明CA4P能够在体外抑制U87细胞的迁移能力,CA4P浓度为50 nmol/L和100 nmol/L能显著抑制迁移(P<0.001)。不同浓度的CA4P作用细胞24 h后,E-Cadherin的蛋白水平随着CA4P的浓度增加而增高。Path Scan结果表明,细胞内信号通路Akt, Bad, SAPK/JNK, S6 ribosomal Protein被激活。结论CA4P能够抑制人U87细胞的增殖和迁移,并且可能与Akt, Bad, SAPK/JNK的上调和S6 ribosomal Protein下调有关。Objective To explore the effect of drug combretast sodium phosphate (CA4P) on the proliferation and migration ofhuman glioma U87 cells and related signaling pathways. Methods U87 cells were cultured in vitro and treated with differentconcentrations of CA4P. The effects of different concentrations of drugs on cell viability were detected by CCK8 assay.Scratches and transwell assays were performed to examine the effect of different drug concentrations on migration of U87 cells.Western blot was used to detect E-Cadherin protein in U87 cells treated with different concentrations. Path Scan to detect theactivation of the pathway. Results The effect of CA4P could inhibit the proliferation of U87 cells in vitro. Scratches andtranswell assays showed that CA4P inhibited the migration of U87 cells in vitro. The concentration of CA4P of 50 nM and 100nM significantly inhibited the migration. After treated with different concentrations of CA4P for 24 h, the protein level of E-Cadherin increased with the increase of CA4P concentration. Path Scan results showed that the intracellular signalingpathways Akt, Bad, SAPK/JNK and S6 ribosomal Protein were activated. Conclusion CA4P can inhibit the proliferation andmigration of human U87 cells, and may be related to the upregulation of Akt, Bad, SAPK/JNK and the downregulation of S6ribosomal protein.
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