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FoxO3a 和尼罗替尼诱导 CML-BC 细胞的红系分化。

FoxO3a and nilotinib-induced erythroid differentiation of CML-BC cells.

机构信息

Department of Hematology, Southeast Hospital of Xiamen University (175 Hospital of Chinese PLA), Zhangzhou, Fujian Province, China.

出版信息

Leuk Res. 2013 Oct;37(10):1309-14. doi: 10.1016/j.leukres.2013.07.001. Epub 2013 Aug 1.

Abstract

We explored the potential involvement of FoxO3a activation in erythroid and granulocytic differentiation for Ph(+) cells of chronic myeloid leukemia blast crisis (CML BC). We demonstrate that FoxO3a activation in CML blast crisis (BC) cells by overexpressing FoxO3a leads to the maturation of CML BC cells. Hemoglobin production significantly increased upon FoxO3a activation in CML BC cells. FoxO3a activation upregulated erythroid surface protein (glycophorin A, GPA), but did not significantly modulate granulocytic markers (CD11b). Additionally, FoxO3a activation reduced the mRNA and protein expression of Tal1. Similar results were observed in cells that were given nilotinib. Our results indicate that FoxO3a activation may promote erythroid differentiation of BC cells via down-regulating Tal1 expression.

摘要

我们探讨了 FoxO3a 激活在慢性髓系白血病急变期(CML BC)Ph(+)细胞的红细胞和粒细胞分化中的潜在作用。我们证明,通过过表达 FoxO3a 激活 CML 急变期(BC)细胞中的 FoxO3a 导致 CML BC 细胞的成熟。在 CML BC 细胞中 FoxO3a 的激活显著增加了血红蛋白的产生。FoxO3a 激活上调了红细胞表面蛋白(糖蛋白 A,GPA),但对粒细胞标志物(CD11b)没有显著调节。此外,FoxO3a 的激活降低了 Tal1 的 mRNA 和蛋白表达。在给予尼洛替尼的细胞中也观察到了类似的结果。我们的结果表明,FoxO3a 的激活可能通过下调 Tal1 表达促进 BC 细胞的红细胞分化。

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