期刊
CELL REPORTS
卷 8, 期 3, 页码 671-677出版社
CELL PRESS
DOI: 10.1016/j.celrep.2014.06.061
关键词
-
类别
资金
- NIH [P01 CA140043, R01 CA78810, R01 CA089720]
- Office of the Assistant Secretary of Defense for Health Affairs through the Prostate Cancer Research Program [W81XWH-13-1-0193]
- Cancer Center Support Grant (CCSG) [CA010815]
Reprogramming of metabolic pathways contributes to human disease, especially cancer, but the regulators of this process are unknown. Here, we have generated a mouse knockout for the mitochondrial chaperone TRAP-1, a regulator of bioenergetics in tumors. TRAP-1(-/-) mice are viable and showed reduced incidence of age-associated pathologies, including obesity, inflammatory tissue degeneration, dysplasia, and spontaneous tumor formation. This was accompanied by global upregulation of oxidative phosphorylation and glycolysis transcriptomes, causing deregulated mitochondrial respiration, oxidative stress, impaired cell proliferation, and a switch to glycolytic metabolism in vivo. These data identify TRAP-1 as a central regulator of mitochondrial bioenergetics, and this pathway could contribute to metabolic rewiring in tumors.
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