白细胞介素 6 和 JAK2/STAT3 信号通路介导地塞米松撤药后 7TD1 多发性骨髓瘤细胞中地塞米松耐药的逆转。
Interleukin-6 and JAK2/STAT3 signaling mediate the reversion of dexamethasone resistance after dexamethasone withdrawal in 7TD1 multiple myeloma cells.
机构信息
Department of Internal Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, MO 63110, USA.
出版信息
Leuk Res. 2013 Oct;37(10):1322-8. doi: 10.1016/j.leukres.2013.06.026. Epub 2013 Jul 18.
Abstract
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.
摘要
我们之前报道了从依赖 IL6 的小鼠 B 细胞杂交瘤 7TD1 细胞系中建立的 DXM 抗性细胞系（7TD1-DXM）的建立和特征。在将 DXM 从 7TD1-DXM 细胞中撤出超过 90 天后，与 7TD1-DXM 细胞相比，DXM 明显抑制了细胞生长并诱导了细胞凋亡（7TD1-WD）。此外，IL-6 逆转，而 IL-6 抗体和 AG490 增强了 DXM 在 7TD1-WD 细胞中诱导的生长抑制和凋亡作用。我们的研究表明，7TD1-DXM 细胞在 DXM 撤出后对 DXM 重新敏感，而 IL-6 和 JAK2/STAT3 途径可能调节这种现象。
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