Is Reliance on Mitochondrial Respiration a "Chink in the Armor" of Therapy-Resistant Cancer?

被引:62
|
作者
Wolf, Dieter A. [1 ]
机构
[1] Sanford Burnham Med Res Inst, Tumor Initiat & Maintenance Program, Degenerat Dis Program, La Jolla, CA 92037 USA
关键词
UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS; ELECTRON-TRANSPORT CHAIN; OXIDATIVE STRESS; SECRETORY PHENOTYPE; CELLULAR SENESCENCE; MELANOMA-CELLS; STEM-CELLS; MECHANISMS; DEATH;
D O I
10.1016/j.ccell.2014.10.001
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A series of recent reports has suggested PGC1 alpha-driven upregulation of mitochondrial oxidative phosphorylation as a selective vulnerability of drug-resistant cancers. Accordingly, chemical inhibitors of respiration led to selective eradication of such cancer cells due to their preferential sensitivity to mitochondrial production of reactive oxygen species. These insights create a timely opportunity for a biomarker guided application of already existing and newly emerging mitochondrial inhibitors in recurrent drug-resistant cancer, including lymphomas, melanomas, and other malignant diseases marked by increased mitochondria! respiration.
引用
收藏
页码:788 / 795
页数:8
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