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- W2527660025 abstract "Metastatic disease is responsible for over 90% of cancer mortality. In breast cancer, the major secondary lesion sites are the lungs, bones, brain, and liver. Small molecule screening and comparative flux studies revealed metabolic heterogeneity in human triple-negative breast cancer MDA-MB-231-derived metastatic subclones that were isolated from the lungs (LM), bones (BoM), and brain (BrM). Oxygen consumption was significantly reduced in LM and BoM, relative to MDA-231 and BrM cells. The extracellular acidification/glycolytic rates were comparable among the cell lines. The mitochondria electron transport chain retained functionality in LM cells, but appeared dysfunctional in BoM and BrM cells. Incorporation of oxidative phosphorylation into its cellular metabolic portfolio afforded LM cells an apparent growth advantage and immunity from glucose depletion, but made LM cells more susceptible to mitochondria-targeted metabolic disruptors. The observed metabolic diversity suggests that organ-dependent metabolic plasticity may serve as a new means to selectively target metastases." @default.
- W2527660025 created "2016-10-07" @default.
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- W2527660025 date "2015-06-25" @default.
- W2527660025 modified "2023-09-27" @default.
- W2527660025 title "Small molecule screening links metabolic plasticity with the target organ selectivity of triple-negative breast tumor metastases" @default.
- W2527660025 doi "https://doi.org/10.1055/s-0035-1556256" @default.
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