期刊文献+
共找到2篇文章
< 1 >
每页显示 20 50 100
Arsenic Trioxide Induces Apoptosis of Glucocorticoid-Resistant Acute Lymphoblastic Leukemia CEM-C1 Cells 被引量:1
1
作者 Jiao Ge Xia Guo Zhi-gui Ma Ling Gu Qiang Li 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2009年第3期217-223,共7页
Objective: To explore the effects of arsenic trioxide (ATO) on the apoptosis of glucocorticoid (GC)-resistant T-acute lymphoblastic leukemia (ALL) CEM-C1 cells and its possible mechanisms. Methods: Different ... Objective: To explore the effects of arsenic trioxide (ATO) on the apoptosis of glucocorticoid (GC)-resistant T-acute lymphoblastic leukemia (ALL) CEM-C1 cells and its possible mechanisms. Methods: Different concentrations of ATO (0.25 μmol/L-5 μmol/L) were used to induce the apoptosis of CEM-C1 cells. The inhibition rate of cell proliferation and apoptosis were detected by MTT test, Annexin V-FITC/PI flow cytometry and optical microscopy, respectively. RT-PCR was applied to semi-quantitatively analyze the mRNA expression of pro-apoptotic proteins (Bad and PDCD4) and anti-apoptotic proteins (XIAP and MCL-1) induced by different concentrations of ATO at different time points. Results: ATO could inhibit proliferation and induce apoptosis of CEM-C1 cells at a concentration and time dependent manner. Low-dose ATO mildly inhibited the proliferation of CEM-C1 cells while higher concentrations (1 μmol/L and 5 μmol/L) had strong anti-tumor effect with the inhibiting rates of 40.07±7.98% and 88.67±2.88%, respectively. Annexin V-FITC/PI flow cytometry showed that the apoptotic rates of CEM-C1 ceils were significantly increased after 48 hours treatment of different concentrations of ATO. RT-PCR demonstrated up-regulated mRNA expression of pro-apoptotic protein Bad and PDCD4 but down-regulated mRNA expression of anti-apoptotic protein XIAP when CEM-C1 cells were treated with different concentrations of ATO at different time points. The MCL-1 mRNA expression was down-regulated only after the treatment of 5 μmol/L ATO. Conclusion: ATO can inhibit cell proliferation and induce cell apoptosis in GC-resistant CEM-C1 cells. The molecular mechanisms might involve the increased mRNA expression of pro-apoptotic protein Bad and PDCD-4, and rapid down-regulation of XIAP mRNA expression. 展开更多
关键词 Acute lymphoblastic leukemia cem-c1 cells APOPTOSIS arsenic trioxide (ATO)
下载PDF
微小RNA⁃34a调控儿童急性淋巴细胞白血病细胞CEM/C1生长和迁移的分子机制研究 被引量:4
2
作者 侯秋苹 任妍 +1 位作者 付敏 张丽丽 《安徽医药》 CAS 2020年第12期2512-2515,共4页
目的研究微小RNA⁃34a(miR⁃34a)对儿童急性淋巴细胞白血病(ALL)细胞CEM/C1增殖、迁移的影响以及可能作用机制。方法选取重庆市第十三人民医院血液科2017年10月至2018年12月住院32例ALL病儿骨髓样本。另选取该院同期25例原发性血小板减少... 目的研究微小RNA⁃34a(miR⁃34a)对儿童急性淋巴细胞白血病(ALL)细胞CEM/C1增殖、迁移的影响以及可能作用机制。方法选取重庆市第十三人民医院血液科2017年10月至2018年12月住院32例ALL病儿骨髓样本。另选取该院同期25例原发性血小板减少症病儿的骨髓样本作为对照组。实时荧光定量多聚核苷酸链式反应(qPCR)检测miR⁃34a在ALL骨髓样本的表达量;CEM/C1细胞按随机数字表法分为对照组、阴性对照(NC)组、miR⁃34a组;对照组细胞常规培养,NC组和miR⁃34a组CEM/C1细胞分别在Lipofectamine 2000介导下转染阴性对照质粒以及miR⁃34a模拟物,qPCR检测转染效率;细胞计数试剂盒8(CCK⁃8)实验检测CEM/C1细胞的增殖,Transwell检测细胞迁移;在线软件TargetScan预测miR⁃34a与Krüppel样因子4(KLF4)的靶向关系,双荧光素酶报告基因进一步进行验证。结果与对照组相比,ALL骨髓样本中miR⁃34a的表达量下调[(0.33±0.05)比(1.00±0.08),t=15.680,P<0.001]。与对照组(1.00±0.08)相比,NC组miR⁃34a的表达量(0.99±0.08)无明显变化,miR⁃34a组CEM/C1细胞中miR⁃34a的表达量(3.21±0.23)上调(F=423.135,P<0.05)。对照组、NC组、miR⁃34a组细胞培养48 h后细胞活性分别为(0.65±0.05)、(0.69±0.06)、(0.42±0.04),F=40.818,P<0.001;迁移细胞数分别为(142.36±12.47)个、(137.45±13.49)个、(79.89±6.23)个,F=57.683,P<0.001,差异有统计学意义。与NC与KLF4⁃wt共转染的细胞相比,miR⁃34a与KLF4⁃wt共转染的细胞荧光素酶活性[(0.45±0.03)比(1.00±0.06),t=20.083,P<0.001]降低;与NC与KLF4⁃mut共转染的细胞相比,miR⁃34a与KLF4⁃mut共转染的细胞荧光素酶活性差异无统计学意义[(1.03±0.07)比(1.01±0.07),t=0.495,P>0.05]。结论miR⁃34a在ALL中表达量下调,其可通过对靶基因KLF4的调控影响CEM/C1细胞增殖、迁移。 展开更多
关键词 白血病 转染 细胞增殖 急性淋巴细胞白血病 人急性淋巴细胞白血病细胞CEM/C1 微小RNA⁃34a Krüppel样因子4 儿童
下载PDF
上一页 1 下一页 到第
使用帮助 返回顶部