期刊
ONCOTARGET
卷 6, 期 40, 页码 42651-42660出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.4765
关键词
EMT; breast cancer; metabolism; metabolic reprogramming; LC-MS metabolomics
资金
- Alkek Center for Molecular Discovery (ACMD)
- [KG110818]
- [DMS 1161759]
- [RP120092]
- [R21-CA185516-01]
- [U01CA179674-01A1]
- [RP-130485 NIH/NCI CA155243]
- Direct For Mathematical & Physical Scien
- Division Of Mathematical Sciences [1545277] Funding Source: National Science Foundation
Metabolic reprogramming is a hallmark of cancer. Epithelial-mesenchymal transition (EMT) induces cancer stem cell (CSC) characteristics and promotes tumor invasiveness; however relatively little is known about the metabolic reprogramming in EMT. Here we show that breast epithelial cells undergo metabolic reprogramming following EMT. Relative to control, cell lines expressing EMT transcription factors show >= 1.5-fold accumulation of glutamine, glutamate, beta-alanine and glycylleucine as well as >= 1.5-fold reduction of phosphoenolpyruvate, urate, and deoxycarnitine. Moreover, these metabolic alterations were found to be predictive of overall survival (hazard ratio = 2.3 (95% confidence interval: 1.31-4.2), logrank p-value = 0.03) and define breast cancer molecular subtypes. EMT-associated metabolites are primarily composed of anapleurotic precursors, suggesting that cells undergoing EMT have a shift in energy production. In summary, we describe a unique panel of metabolites associated with EMT and demonstrate that these metabolites have the potential for predicting clinical and biological characteristics associated with patient survival.
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