期刊
NATURE COMMUNICATIONS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms8530
关键词
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资金
- National Institutes of Health through The University of Texas MD Anderson Cancer Center's Support Grant [CA016672]
- National Cancer Institute [RO1CA 089266]
- Fidelity Foundation
- Directed Medical Research Programs Department of Defense Synergistic Idea Development Award [BC062166]
- Susan G. Komen Breast Cancer Research Foundation Promise Grant
- CPRIT grant [RP101243-P5]
- Vietnam Education Foundation
- Rosalie B. Hite Foundation
- Department of Defense Breast Cancer Research Program [W81XWH-10-0171]
- MD Anderson Cancer Center Training Grant Program in Molecular Genetics [NIH T32CA009299]
- cancer prevention fellowship [NIH R25T CA57730]
- National Cancer Institute grant minority supplement [NIH R01CA089266]
Extensive reprogramming of cellular energy metabolism is a hallmark of cancer. Despite its importance, the molecular mechanism controlling this tumour metabolic shift remains not fully understood. Here we show that 14-3-3 sigma regulates cancer metabolic reprogramming and protects cells from tumorigenic transformation. 14-3-3 sigma opposes tumour-promoting metabolic programmes by enhancing c-Myc poly-ubiquitination and subsequent degradation. 14-3-3 sigma demonstrates the suppressive impact on cancer glycolysis, glutaminolysis, mitochondrial biogenesis and other major metabolic processes of tumours. Importantly, 14-3-3 sigma expression levels predict overall and recurrence-free survival rates, tumour glucose uptake and metabolic gene expression in breast cancer patients. Thus, these results highlight that 14-3-3 sigma is an important regulator of tumour metabolism, and loss of 14-3-3 sigma expression is critical for cancer metabolic reprogramming. We anticipate that pharmacologically elevating the function of 14-3-3 sigma in tumours could be a promising direction for targeted anticancer metabolism therapy development in future.
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