期刊
MOLECULAR CELL
卷 70, 期 3, 页码 502-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2018.03.029
关键词
-
资金
- NIH [CA123391, CA166575, CA163591, CA188096, CA130893]
- NSF/NIH/DoE [DBI-1338415]
- National Natural Science Foundation of China [81372564, 81372600, 81572440, 81671148, 81730081]
- Natural Science Foundation of Guangdong Province for Distinguished Young Scholars [2015A030306047]
- Research Fund of State Key Laboratory of Oncology in South China
- Rutgers Cancer Institute of New Jersey Shared Resources for Advanced Microscopy
- Biomedical Informatics
- Biometrics, Biospecimen Repository and Histopathology Service
- Flow Cytometry/Cell Sorting (NIH) [P30 CA072720]
Nutrients are not only organic compounds fueling bioenergetics and biosynthesis, but also key chemical signals controlling growth and metabolism. Nutrients enormously impact the production of reactive oxygen species (ROS), which play essential roles in normal physiology and diseases. How nutrient signaling is integrated with redox regulation is an interesting, but not fully understood, question. Herein, we report that superoxide dismutase 1 (SOD1) is a conserved component of the mechanistic target of rapamycin complex 1 (mTORC1) nutrient signaling. mTORC1 regulates SOD1 activity through reversible phosphorylation at S39 in yeast and T40 in humans in response to nutrients, which moderates ROS level and prevents oxidative DNA damage. We further show that SOD1 activation enhances cancer cell survival and tumor formation in the ischemic tumor microenvironment and protects against the chemotherapeutic agent cisplatin. Collectively, these findings identify a conserved mechanism by which eukaryotes dynamically regulate redox homeostasis in response to changing nutrient conditions.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据