分析硫代氨基卡巴松复合物对Jurkat E6.1急性淋巴性白血病细胞系UCA1 lncRNA和AKT靶点的影响、基因表达改变、调控PI3K/ AKT信号通路

faranak daneshi, F. Ghorbani, golnaz asadi tehrani, azadeh mirza ahmadi
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引用次数: 0

摘要

背景与目的:白血病通常起源于骨髓,并导致大量异常白细胞的产生。本研究旨在探讨硫代氨基脲配合物(镍)对Jurkat E6.1急性淋巴性白血病细胞UCA1 lncRNA和AKT靶点、基因表达变化、PI3K/ AKT信号通路的调控作用。材料与方法:首先,以不同浓度(0.5、1、2、5大分子)和(1、5、10、25大分子)提供硫代氨基脲配合物Ni和6MP,在细胞传代后(24 ~ 48 ~ 72h)用上述剂量处理jurkat E.6.1癌细胞。下一步进行RNA提取和cDNA合成,Real Time PCR检测UCA1和AKT基因的表达。最后,利用Rest软件对结果进行分析。结果:6mp浓度(1、5、10和25大分子)治疗24h后,UCA1显著降低(P<0.001)。在镍中,在2和5大分子浓度下,在72小时内观察到明显的下降。6mp处理24h时,5、10和25macromolecular浓度的AKT和72h时,所有浓度(1、5、10和25macromolecular)均显著降低(P<0.001)。在0.5、1、2和5大分子浓度的镍中,24小时的表达量下降,0.5μ m浓度的表达量下降无统计学意义。(2和5大分子)在48和72小时显著降低(P<0.001)。结论:6mp和镍治疗后UCA1和AKT的表达变化与给药时间和浓度有关。UCA1在6MP处理25μM和24小时,镍处理5μM和72小时,AKT在6MP处理25μM和72小时,镍处理5μM和24小时,由于基因表达,对细胞的影响最大。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Analysis of thiosemi carbazon complexes effects on UCA1 lncRNA and AKT target, gene expression alternations, regulating PI3K/ AKT signaling pathway in Jurkat E6.1 Acute Lympholastic Leukemia cell line
Background and Aim:Leukemia usually begins in the bone marrow and leads to the production of a large number of abnormal white blood cells.The goal of this study was to investigate changes on UCA1 lncRNA and AKT target, gene expression alternations, regulating PI3K/ AKT signaling pathway in Jurkat E6.1 Acute Lympholastic Leukemia cell line under treatment with thiosemicarbazone complexes(nickel). Materials and Methods: First, thiosemicarbazones complex Ni and 6MP was provided in different concentrations(0.5,1,2,5macromolecular)and(1,5,10,25macromolecular) and the jurkat E.6.1 Cancer cells were treated with mentioned doses at (24-48-72hours)after cell passage. Next RNA extraction and cDNA synthesis were performed and the expression of UCA1 and AKT gene were appraised by Real Time PCR. Finally, the results were analyzed by Rest Software. Results:UCA1 showed a significant decrease during 24hours of treatment with 6mp at concentrations(1,5,10and25macromolecular)(P<0.001).In nickel,a significant decrease at 72hours was observed at concentrations(2and 5macromolecular).in the AKT in treatment with 6mp at 24hours At concentrations(5,10and 25macromolecular)And all concentrations(1,5,10and25macromolecular)at 72hours showed a significant decrease(P<0.001).In nickel at concentrations(0.5,1,2and5macromolecular)at 24hours Decreased expression was observed,This decrease is not statistically significant at a concentration of 0.5μM.at concentrations(2and 5macromolecular)Significant reductions at 48and72hours were observed(P<0.001). Conclusion:UCA1 and AKT expression changes after treatment with 6mp and nickel depend on drug timing and concentration.UCA1 in 6MP treatment at 25μM and 24hours,in treatment with nickel at 5μM and 72hours , AKT in 6mp treatment at 25μM and 72hours , In treatment with nickel at 5μM and 24hours,It had the highest effect on the cell due to gene expression.
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