TBK1 Activation by VHL Loss in Renal Cell Carcinoma: A Novel HIF-Independent Vulnerability

被引:10
作者
Bakouny, Ziad [1 ]
Barbie, David A. [1 ,2 ]
机构
[1] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA
[2] Dana Farber Canc Inst, Belfer Ctr Appl Canc Sci, Boston, MA 02115 USA
关键词
D O I
10.1158/2159-8290.CD-19-1525
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
The Von Hippel-Lindau gene product is a tumor suppressor whose ubiquitin ligase function is key to oxygen-sensing in cells, whereas Tank-binding kinase (TBK1) is a kinase mostly implicated in innate immune response. The study by Hu and colleagues in this issue reveals that VHL suppresses TBK1 activity under normoxic conditions, and that loss of VHL in kidney cancer cells renders them sensitive to TBK1 inhibition, providing a new potential target for the treatment of clear cell renal cell carcinoma.
引用
收藏
页码:348 / 350
页数:3
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