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拉巴胺通过调节mTORC1通路介导的亡和自性来增加白血病细胞对化疗的敏感性

Jing Xu¹, Siwen Zong², Tianle Sheng³

¹Department of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.

International journal of hematology

|March 26, 2024

概括

在急性髓性白血病 (AML) 模型中,与化疗相结合的拉巴胺显示出增强的抗白血病效应. 这种组合疗法促进了亡和自,为AML治疗提供了一个有前途的策略.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

急性髓性白血病 (AML) 仍然是血液恶性瘤的一个重大挑战.
针对AML的标准化疗方案可能与耐药性和毒性有关.
正在探索有针对性的疗法,以提高AML治疗疗效.

研究的目的:

调查单独使用拉巴胺和与多克索鲁比和细胞氨基酸化疗联合使用的拉巴胺对AML的疗效.
阐明拉帕米在AML中的作用的潜在分子机制.
评估拉巴胺与AML治疗中的标准化疗的协同作用潜力.

主要方法:

在体外研究中使用人类急性单细胞白血病细胞系SHI-1.
使用NPG AML小鼠模型进行体内研究.
细胞增殖试验 (细胞计数套装-8).
西部斑点,流细胞计和免疫组织化学分析.

主要成果:

拉帕米辛和化疗都在体外抑制了SHI-1细胞的增殖,并在体内抑制了瘤的生长.
与单独治疗相比,Rapamycin和化疗的组合显示出更好的抗瘤效果.
拉帕米辛治疗通过调节mTORC1通路中的蛋白质 (例如,增加Bax,Beclin-1,LC3B-II,ATG5;减少Bcl-2) 导致了亡和自的增加.

结论:

拉帕米辛在AML治疗中表现出与多克索鲁比辛和细胞氨基酸的协同作用.
组合疗法促进癌细胞亡和自.
mTORC1通路涉及拉帕素在AML中的作用机制.

关键词:

在4EBP1中.细胞灭亡 (apoptosis) 是一种死亡的过程.在白血病中,白血病.拉帕米辛是一种可怕的药物.这就是S6K1的原因.在mTOROR中使用mTOR.

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