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首页> 外文期刊>Leukemia Research: A Forum for Studies on Leukemia and Normal Hemopoiesis >Interleukin-6 and JAK2/STAT3 signaling mediate the reversion of dexamethasone resistance after dexamethasone withdrawal in 7TD1 multiple myeloma cells
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Interleukin-6 and JAK2/STAT3 signaling mediate the reversion of dexamethasone resistance after dexamethasone withdrawal in 7TD1 multiple myeloma cells

机译:在7TD1多发性骨髓瘤细胞中撤除地塞米松后,白介素6和JAK2 / STAT3信号传导介导地塞米松耐药的逆转

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摘要

We previously reported the establishment and characteristics of a DXM-resistant cell line (7TD1-DXM) generated from the IL6-dependent mouse B cell hybridoma, 7TD1 cell line. After withdrawing DXM from 7TD1-DXM cells over 90 days, DXM significantly inhibited the cell growth and induced apoptosis in the cells (7TD1-WD) compared with 7TD1-DXM cells. Additionally, IL-6 reversed while IL-6 antibody and AG490 enhanced the effects of growth inhibition and apoptosis induced by DXM in 7TD1-WD cells. Our study demonstrates that 7TD1-DXM cells become resensitized to DXM after DXM withdrawal, and IL-6 and JAK2/STAT3 pathways may regulate the phenomenon.
机译:我们先前报道了从依赖IL6的小鼠B细胞杂交瘤7TD1细胞系产生的DXM耐药细胞系(7TD1-DXM)的建立和特性。与7TD1-DXM细胞相比,从7TD1-DXM细胞撤出DXM 90天后,DXM显着抑制了细胞生长并诱导了细胞凋亡(7TD1-WD)。另外,IL-6反向,而IL-6抗体和AG490增强了DXM诱导的7TD1-WD细胞生长抑制和凋亡的作用。我们的研究表明,撤回DXM后7TD1-DXM细胞对DXM重新敏感,并且IL-6和JAK2 / STAT3途径可能调节了该现象。

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