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• W2125715541 abstract "Metabolic alterations, driven by genetic and epigenetic factors, have long been known to be associated with the etiology of cancer. Furthermore, accumulating evidence suggest that cancer metabolism is intimately linked to drug resistance, which is currently one of the most important challenges in cancer treatment. Altered metabolic pathways help cancer cells to proliferate at a rate higher than normal, adapt to nutrient limited conditions, and develop drug resistance phenotypes. Application of systems biology, boosted by recent advancement of novel high-throughput technologies to obtain cancer-associated, transcriptomic, proteomic and metabolomic data, is expected to make a significant contribution to our understanding of metabolic properties related to malignancy. Indeed, despite being at a very early stage, quantitative data obtained from the omics platforms and through applications of (13)C metabolic flux analysis (MFA) in in vitro studies, researchers have already began to gain insight into the complex metabolic mechanisms of cancer, paving the way for selection of molecular targets for therapeutic interventions. In this review, we discuss some of the major findings associated with the metabolic pathways in cancer cells and also discuss new evidences and achievements on specific metabolic enzyme targets and target-directed small molecules that can potentially be used as anti-cancer drugs." @default.
• W2125715541 created "2016-06-24" @default.
• W2125715541 creator A5035240428 @default.
• W2125715541 creator A5037171791 @default.
• W2125715541 date "2015-09-30" @default.
• W2125715541 modified "2023-10-01" @default.
• W2125715541 title "Cancer Metabolism and Drug Resistance" @default.
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• W2125715541 doi "https://doi.org/10.3390/metabo5040571" @default.
• W2125715541 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4693186" @default.

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