SDHA
癌症研究
肝细胞癌
生物
下调和上调
化学
琥珀酸脱氢酶
细胞生物学
生物化学
线粒体
基因
作者
Tao Yuan,Tianyi Zhou,Meijia Qian,Jiamin Du,Yue Liu,Jia’er Wang,Yonghao Li,Guanghan Fan,Fangjie Yan,Xiaoyang Dai,Xiawei Li,Yulian Wu,Xin Dong,Qiaojun He,Hong Zhu,Bo Yang
出处
期刊:Hepatology
[Lippincott Williams & Wilkins]
日期:2022-06-17
卷期号:78 (1): 103-119
被引量:31
摘要
Our study demonstrated that SDHA/B reduction promotes HCC proliferation by preventing the proteasomal degradation of YAP/TAZ through modulating cullin1 NEDDylation, thus binding SDH-deficient HCC cells to YAP/TAZ pathway and rendering these cells vulnerable to YAP/TAZ inhibition. Our findings warrant further investigation on the therapeutic effects of targeting YAP/TAZ in patients with HCC displaying reduced SDHA/B or elevated succinate levels.
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