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作 者:郑润桃[1] 庄敏丽 张文霞[1] ZHENG Runtao;ZHUANG Minli;ZHANG Wenxia(Department of Blood Transfusion,Inner Mongolia Medical University Affiliated Hospital,Hohhot,010050,China)
机构地区:[1]内蒙古医科大学附属医院输血科,呼和浩特市010050
出 处:《医学分子生物学杂志》2024年第5期413-418,共6页Journal of Medical Molecular Biology
基 金:内蒙古自治区自然科学基金(No.2022WZ01)。
摘 要:目的研究积雪草苷对慢性粒细胞白血病(chronic myelogenous leukemia,CML)细胞增殖、迁移和周期停滞的作用,并且探讨了其对GATA-1表达的调节。方法以CML细胞系K562、抗伊马替尼(imatinib,IM)K562细胞(K562r)和人源CML细胞为模型,CCK-8测定不同浓度积雪草苷对3种细胞活力的影响。选择0、25、50、100μmol/L积雪草苷处理K562r细胞,CFSE标记测定细胞增殖,Transwell测定细胞迁移,流式细胞仪检测细胞周期,蛋白质印迹检测cyclin A、CDK2、CDK4、cyclin D1、Ki67、PCNA、VEGF、MMP-9和MMP-14蛋白水平。结果与对照组比较,积雪草苷处理可显著抑制K562r细胞增殖和迁移,并促进其细胞周期阻滞。同时我们发现积雪草苷处理可显著上调K562r细胞中GATA-1水平。结论积雪草苷能够抑制K562r细胞增殖、迁移并诱导其细胞周期阻滞,其机制可能与GATA-1的表达上调相关。Objective To study the effect of asiaticoside on the proliferation,invasion and cell cycle arrest of chronic myelogenous leukemia(CML)cells,and to explore its regulation on GATA-1 expression.Methods CML cell line K562,imatinib(IM)-resistant K562 cells(K562r)and human original CML cells were used for experiments.Cell viability was determined by CCK-8 assay.K562r cells were treated with 0,25,50,100μmol/L asiaticoside,then cell proliferation was determined by colony formation assay,cell migration was determined by transwell assay,the cell cycle was measured by flow cytometry,the expression levels of cyclin A,CDK2,CDK4,cyclin D1,Ki67,PCNA,VEGF,MMP-9 and MMP-14 were detected by Western blotting.Results Compared with the control group,asiaticoside treatment significantly reduced the number of K562r cell colonies and migration cells,and induced the cell cycle arrest.In addition,the expression level of GATA-1 in K562r cells was significantly up-regulated after asiaticoside treatment.Conclusion Asiaticoside can inhibit the proliferation and migration of K562r cells and induce cell cycle arrest,and the mechanism may be related to the up-regulation of GATA-1 expression.
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