Acquired temozolomide resistance in MGMT-deficient glioblastoma cells is associated with regulation of DNA repair by DHC2

Acquired temozolomide resistance in MGMT-deficient glioblastoma cells is associated with regulation of DNA repair by DHC2
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MGMT 缺陷的胶质母细胞瘤细胞获得性替莫唑胺耐药与 DHC2 调节 DNA 修复有关

DOI:
10.1093/brain/awz202
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发表时间:
2019-08-01
期刊:
影响因子:
14.5
通讯作者:
Qi, Songtao
Qi, Songtao
中科院分区:
医学1区
文献类型:
--
作者:
Yi, Guo-Zhong;Huang, Guanglong;Qi, Songtao

文献摘要

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相似文献

MGMT缺陷型胶质母细胞瘤对替莫唑胺产生耐药性的机制尚不清楚。Yi等人表明,DNA损伤修复蛋白XPC和CBX 5的逆行核转运在MGMT缺陷型胶质母细胞瘤细胞中赋予替莫唑胺抗性。DHC2抑制剂的开发可能是克服获得性替莫唑胺耐药性的一种有前途的策略。
The mechanisms by which MGMT-deficient glioblastomas acquire resistance to temozolomide are unclear. Yi et al. show that retrograde nuclear transportation of the DNA damage repair proteins XPC and CBX5 confers temozolomide resistance in MGMT-deficient glioblastoma cells. Development of DHC2 inhibitors could be a promising strategy for overcoming acquired temozolomide resistance.