Abstract
Cancer cells possess unique metabolic signatures compared to normal cells, including shifts in aerobic glycolysis, glutaminolysis, and de novo biosynthesis of macromolecules. Targeting these changes with agents (drugs and dietary components) has been employed as strategies to reduce the complications associated with tumorigenesis. This paper highlights the ability of several food components to suppress tumor-specific metabolic pathways, including increased expression of glucose transporters, oncogenic tyrosine kinase, tumor-specific M2-type pyruvate kinase, and fatty acid synthase, and the detection of such effects using various metabonomic technologies, including liquid chromatography/mass spectrometry (LC/MS) and stable isotope-labeled MS. Stable isotope-mediated tracing technologies offer exciting opportunities for defining specific target(s) for food components. Exposures, especially during the early transition phase from normal to cancer, are critical for the translation of knowledge about food components into effective prevention strategies. Although appropriate dietary exposures needed to alter cellular metabolism remain inconsistent and/or ill-defined, validated metabonomic biomarkers for dietary components hold promise for establishing effective strategies for cancer prevention.
Highlights
Cancer cells exhibit unique metabolic signatures that are required for their aberrant proliferation [1]
Isothiocyanates in broccoli have been reported to inhibit tyrosine kinases (TKs) [28]. These findings suggest that some of the antiproliferative effects of bioactive food components may arise from their ability to convert tetrameric PKM2 to dimeric PKM2 and thereby bring about a shift in glucose flux from a nonoxidative to an oxidative pathway
Differential glucose metabolic pathways between normal and cancer cells in lung: 13C glucose was infused to lung cancer patients and showed enhanced production of Asp and Glu via glycolysis in lung tumor tissues
Summary
Cancer cells exhibit unique metabolic signatures that are required for their aberrant proliferation [1]. It is important to develop a standardized format that allows the scientific community to understand results from studies with widely different conditions. To facilitate this process, a working group of the Metabolomics Standards Initiative was formed in 2004 [14]. Considerable evidence points to diet as a variable that can influence cancer risk and/or tumor behavior [16] This dietary effect may arise from its interactions with key regulatory molecules in various cancer processes, including carcinogen metabolism, hormonal balance, cell signaling, cell cycle control, apoptosis, and differentiation. This is critical to evaluate whether a single or multiple dietary component(s) modulate the early transition phase from normal to cancer phenotypes, including changes in specific enzymatic activities and carbon flows
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