程序性细胞死亡
癌细胞
线粒体
电压依赖性阴离子通道
生物
癌症
VDAC1型
线粒体分裂
细胞生物学
调节器
细胞
癌症研究
细胞凋亡
遗传学
基因
细菌外膜
大肠杆菌
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2019-12-13
卷期号:79 (24): 6074-6075
被引量:8
标识
DOI:10.1158/0008-5472.can-19-3276
摘要
Abstract Carefully orchestrated interactions between mitochondrial proteins that facilitate cell death remain a topic of intense research, however, key steps remain to be elucidated, especially those that drive selective killing in cancer cells. How mitochondrial dysfunction and its regulation in cancer can be robustly leveraged for anticancer cell killing in a heterogeneous population of cells within a tumor also remains a promising but unfulfilled premise. Toward this goal, in this issue of Cancer Research, Seo and colleagues have identified the protein complex between mitochondrial fission factor (MFF1 and MFF2) and voltage-dependent anion channel (VDAC1) as a novel regulator of mitochondrial cell death and a potential target for selective cancer cell killing. See related article by Seo et al., p. 6215
科研通智能强力驱动
Strongly Powered by AbleSci AI