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出 处:《现代生物医学进展》2014年第18期3418-3421,共4页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(21175092;21105064);国家重大科学仪器设备开发专项(2011YQ150072;2011YQ15007204;2011YQ15007207;2011YQ15007210);上海市自然科学基金项目(12ZR1413600)
摘 要:目的:以药物干预前后的Jurkat细胞为样本,旨在找出能够有效干预淋巴瘤的药物及与淋巴瘤相关的代谢及信号通路。方法:以UPLC-3Q MS为技术平台,通过多反应监测(Multiple Reaction Monitoring,MRM)扫描模式,根据实验室前期淋巴瘤代谢组学的研究成果,选择对淋巴瘤患者和健康对照组分类有显著贡献的脂类差异代谢物作为监测对象,对PI3K inhibitor干预前后的Jurkat细胞内这些潜在的生物标记物进行定量研究。结果:PI3K inhibitor与Jurkat细胞作用一段时间后,所监测的四个脂质代谢物含量呈现出与药物干预前肿瘤组相反的变化趋势,药物干预后细胞内含量有明显先升高再降低的趋势。结论:说明PI3K介导的信号通路在淋巴瘤细胞内被放大,选择性抑制该通路可以有效抑制肿瘤增殖和肿瘤细胞的代谢活动,为淋巴瘤的临床研究提供依据。Objective: To monitor and detect the concentration change of some metabolites in Jurkat cells before and after the drug intervention and to ihd out the signaling pathway that is closely related to the lymphoma. Methods: Based on UPLC-3Q MS platform, Multiple Reaction Monitoring (MRM) Scanning mode was applied to quantify four lipid metabolites in Jurkat cells Which were intervened with PI3K irdtibitor. Then the concerltrations of metabolites in Jurkat cells with and without PI3K inhibitor intervehtion were compared. The lipid metabolites were chosen as the potential biomarkers according to the research achievements of previous lymphoma metabolomics in our lab, which significantly contribute to the classification of lymphoma patients and healthy controls. Results: After interaction with the PI3K inhibitor, the concentration level of related metabolites in Jurkat cells showed an increase tendency, which was opposite to that of the original cancer cell. Conelusiorts: It illustrates that the PI3K signaling pathway is substantially enhanced in the cancer cell and the inhibition of the PI3K can effectively inhibit the proliferation of the cancer cell.
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