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作 者:葛繁梅[1] 白庆咸[2] 高延慧[1] 刘延香[1]
机构地区:[1]延安大学医学院附属医院血液科,陕西延安716000 [2]第四军医大学西京医院血液科,陕西西安710032
出 处:《基础医学与临床》2008年第2期172-176,共5页Basic and Clinical Medicine
摘 要:目的探讨三氧化二砷(As2O3)对人多发性骨髓瘤细胞系RPMI8226细胞生物学特性影响的分子机制。方法用人多发性骨髓瘤细胞系RPMI8226细胞作为体外实验对象。应用流式细胞仪检测细胞周期、凋亡峰、死亡受体DR4和DR5分子及黏附分子VLA4(CD49d)的表达;用聚合酶链反应测定靶细胞CXCR4基因表达;免疫组化染色和荧光显微镜检测DR4和DR5分子的表达情况。结果5μmol/L的As2O3可以明显上调RPMI8226细胞DR4、DR5分子的表达(P<0.01),明显下调CXCR4基因和VLA4分子表达;还可以诱导RPMI8226细胞凋亡、增加G1期细胞比例,出现明显凋亡峰。结论As2O3诱导RPMI8226细胞凋亡,可能与死亡受体DR4、DR5分子过度表达有关;As2O3抑制靶细胞CXCR4基因和黏附分子VLA4的表达,从而影响细胞的增殖、迁移与归巢能力。Objective To investigate the effect of arsenic trioxide ( As2O3 ) on the biology characteristics of multiple myeloma RPMI8226 ceils in vitro and the molecular mechanism. Methods Multiple myeloma RPMI8226 ceils were used for experiments target, cell cycle, apoptotic peak, and adhesion molecular VLA4 (CIM9d) were determinded by flow cytometry. Expression of CXCR4gene was examined by RT-PCR. Expression of death receptor DR4 and DR5 were measured by immunofluorescence microscopy and flow cytometry. Results Five μmol/L As2O3 upregulated DR4 and DR5 expression on RPMI8226 cells markedly ( P 〈 0. 01 ) down-regulated CXCR4 gene and VLA4 expression. Flow cytometry showed that the proportion of G1 ceils was increased with appearance of apoptosis peak. Conclusion As2O3 induced apoptosis of multiple myeloma RPMI8226 cells in vitro. It may be explained by over-expression of death receptor DR4.DR5 and down-regulated VLA4. As2O3 inhibited CXCR4 expression of RPMI8226 cells, Thereby it affected activity on RPMI8226 cells on proliferation, migration and imigration.
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