期刊
CANCER RESEARCH
卷 77, 期 13, 页码 3391-3405出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-16-0425
关键词
-
类别
资金
- NIH [1R01CA137494, R01CA132115, R01CA086072]
- Sidney Kimmel Cancer Center NIH Cancer Center Core grant [P30CA056036]
- Breast Cancer Research Foundation
- Dr. Ralph and Marian C. Falk Medical Research Trust
- Pennsylvania Department of Health
- American-Italian Cancer Foundation Post-doctoral Research Fellowship
Autophagy activated after DNA damage or other stresses mitigates cellular damage by removing damaged proteins, lipids, and organelles. Activation of the master metabolic kinase AMPK enhances autophagy. Here we report that cyclin D1 restrains autophagy by modulating the activation of AMPK. In cell models of human breast cancer or in a cyclin D1-deficient model, we observed a cyclin D1-mediated reduction in AMPK activation. Mechanistic investigations showed that cyclin D1 inhibited mitochondrial function, promoted glycolysis, and reduced activation of AMPK ( pT172), possibly through a mechanism that involves cyclin D1-Cdk4/Cdk6 phosphorylation of LKB1. Our findings suggest how AMPK activation by cyclin D1 may couple cell proliferation to energy homeostasis. (C)2017 AACR.
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