Interleukin-6 and JAK2/STAT3 signaling mediate the reversion of dexamethasone resistance after dexamethasone withdrawal in 7TD1 multiple myeloma cells
白细胞介素 6 和 JAK2/STAT3 信号转导介导 7TD1 多发性骨髓瘤细胞中地塞米松停药后地塞米松耐药性的逆转
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作者:Tuoen Liu, Zhiqiang Fei, Kalyan J Gangavarapu, Senyo Agbenowu, Alok Bhushan, James C K Lai, Christopher K Daniels, Shousong Cao
| 期刊: | Leukemia Research | 影响因子: | 2.100 |
| 时间: | 2013 | 起止号: | 2013 Oct;37(10):1322-8. |
| doi: | 10.1016/j.leukres.2013.06.026 | 研究方向: | 信号转导 |
| 疾病类型: | 骨髓瘤 | 细胞类型: | 其它细胞 |
| 信号通路: | JAK/STAT | |
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.
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