摘要
测试STAT3基因在人横纹肌肉瘤细胞中的作用,遗传的方法被用来抑制STAT3和GP130的表达,使用短RNA(shRNA)的上端来激活STAT3表达或者持续活跃的STAT3蛋白。细胞GP130 或者 STAT3 表达解除了致敏细胞的抗癌药物阿霉素,顺铂以及MEK抑制剂AZD6244。另一方面,组成性激活的STAT3蛋白表达会降低这些药物横纹肌肉瘤的细胞的敏感性。此外,我们测试了一种小分子STAT3抑制剂LY5和横纹肌肉瘤细胞抑制剂苯卓昔芬GP130。
关键词: STAT3;GP130;横纹肌肉瘤;顺铂;阿霉素;MEK抑制剂。
Current Cancer Drug Targets
Title:Persistent GP130/STAT3 Signaling Contributes to the Resistance of Doxorubicin, Cisplatin, and MEK Inhibitor in Human Rhabdomyosarcoma Cells
Volume: 16 Issue: 7
Author(s): Xiaojuan Wu, Hui Xiao, Ruoning Wang, Lingling Liu, Chenglong Li, Jiayuh Lin
Affiliation:
关键词: STAT3;GP130;横纹肌肉瘤;顺铂;阿霉素;MEK抑制剂。
摘要: To test the role of STAT3 in human rhabdomyosarcoma cells, genetic approaches were used to either knockdown the expression of STAT3 and GP130, an upstream activator of STAT3 using short hairpin RNA (shRNA) or express persistently active STAT3 protein. Knockdown expression of GP130 or STAT3 sensitized cells to anti-cancer drugs doxorubicin, cisplatin, and MEK inhibitor AZD6244. On the other hand, expression of the constitutively active STAT3 protein reduced the sensitivity of rhabdomyosarcoma cells to those drugs.
In addition, we tested a small molecule STAT3 inhibitor LY5 and a GP130 inhibitor bazedoxifene in rhabdomyosarcoma cells. Our data demonstrated that the combination of LY5 or bazedoxifene with doxorubicin, cisplatin, and AZD6244 showed stronger inhibitory effects than single agent alone. In summary, our results demonstrated that GP130/STAT3 signaling contributes to the resistance of these drugs in rhabdomyosarcoma cells. They also suggested a potentially novel cancer therapeutic strategy using the combination of inhibitors of GP130/STAT3 signaling with doxorubicin, cisplatin, or AZD6244 for rhabdomyosarcoma treatments.
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Xiaojuan Wu, Hui Xiao, Ruoning Wang, Lingling Liu, Chenglong Li, Jiayuh Lin , Persistent GP130/STAT3 Signaling Contributes to the Resistance of Doxorubicin, Cisplatin, and MEK Inhibitor in Human Rhabdomyosarcoma Cells, Current Cancer Drug Targets 2016; 16 (7) . https://dx.doi.org/10.2174/1568009615666150916093110
DOI https://dx.doi.org/10.2174/1568009615666150916093110 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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