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• W2914031101 abstract "We have developed a novel therapeutic paradigm (metabolic priming) for cancer whereby restriction of the essential amino acid methionine activates a number of cell-stress-response pathways that can be selectively targeted to enhance the therapeutic impact of methionine restriction. One example of metabolic priming is the combination of methionine restriction with proapoptotic TRAIL receptor-2 (TRAIL-R2) agonists. Methionine restriction enhances the cell surface expression of TRAIL-R2 selectively in transformed breast epithelial cells and renders them more susceptible to cell death induction by TRAIL-R2 agonists in cellular and murine models of breast cancer. This methods review focuses on preclinical models of breast cancer to investigate metabolic priming by methionine restriction. Multiple cell-based methods are detailed to measure cell viability, cell survival, caspase activity, apoptosis, and matrix detachment-induced cell death (anoikis). In addition, we describe an orthotopic model of metastatic breast cancer that utilizes mCherry-fluorescently-labeled human breast cancer cells. This model captures the entire metastatic cascade from the mammary gland to the lung and mimics key features of the human disease. These breast-cancer models can be readily adapted to other tumor types. Overall, we provide a stepwise, translationally-relevant approach to study metabolic priming in the context of cancer." @default.
• W2914031101 created "2019-02-21" @default.
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• W2914031101 date "2019-01-01" @default.
• W2914031101 modified "2023-09-23" @default.
• W2914031101 title "Preclinical Breast Cancer Models to Investigate Metabolic Priming by Methionine Restriction" @default.
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• W2914031101 doi "https://doi.org/10.1007/978-1-4939-8796-2_6" @default.
• W2914031101 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6571148" @default.
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