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首页> 外文期刊>Journal of cellular physiology. >E35 ablates acute leukemia stem and progenitor cells in vitro and in vivo
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E35 ablates acute leukemia stem and progenitor cells in vitro and in vivo

机译：急性白血病干细胞和祖E35脱落细胞在体外和体内

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摘要

Leukemia stem cells (LSCs) have critical functions in acute leukemia (AL) pathogenesis, participating in its initiation and relapse. Thus, identifying new molecules to eradicate LSCs represents a high priority for AL management. This work identified E35, a novel Emodin derivative, which strongly inhibited growth and enhanced apoptosis of AL stem cell lines, and primary stem and progenitor cells from AL cases, while sparing normal hematopoietic cells. Furthermore, functional assays in cultured cells and animals suggested that E35 preferentially ablated primitive leukemia cell populations without impairing their normal counterparts. Moreover, molecular studies showed that E35 remarkably downregulated drug-resistant gene and dramatically inhibited the Akt/ mammalian target of rapamycin signaling pathway. Notably, the in vivo anti-LSC activity of E35 was further confirmed in murine xenotransplantation models. Collectively, these findings indicate E35 constitutes a novel therapeutic candidate for AL, potentially targeting leukemia stem and progenitor cells.
机译：白血病干细胞(lsc)的关键功能在急性白血病(AL)发病机理,参与其起始和复发。因此,确定消除lsc新分子代表一个高优先级的管理。这项工作确定E35,小说大黄素导数,强烈抑制增长增强细胞凋亡的干细胞系主要的干细胞和祖细胞从基地的情况下,的同时,仍能保留正常的造血细胞。此外,在培养细胞功能检测和动物建议E35优先熔化的原始的白血病细胞的数量没有影响正常的同行。此外,研究表明,E35分子值得注意的是耐药基因表达下调显著抑制一种蛋白激酶/哺乳动物的目标雷帕霉素的信号通路。体内anti-LSC E35进一步的活动证实在小鼠异种移植模型。总的来说,这些发现表明E35构成小说治疗候选人,可能针对白血病干细胞和祖细胞。

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