Nutrient utilization is dramatically altered when cells receive signals to proliferate. Characteristic metabolic changes enable
cells to meet the large biosynthetic demands associated with cell growth and division. Changes in rate-limiting glycolytic enzymes redirect
metabolism to support growth and proliferation. Metabolic reprogramming in cancer is controlled largely by oncogenic activation of
signal transduction pathways and transcription factors. Although less well understood, epigenetic mechanisms may seem to contribute to
the regulation of metabolic gene expression in cancer. Reciprocally, accumulating evidence suggests that metabolic alterations may affect
the epigenome. Understanding the relation between metabolism and epigenetics in cancer cells may open new avenues for anti-cancer
In multi-cellular systems, molecular signals promoting cell growth and proliferation mediate the switch between catabolism and anabolism.
Both normal proliferating and cancer cells must achieve high levels of macromolecular biosynthesis to provide the raw materials
needed to produce new daughter cells. From a therapeutic view point, it is of great interest to determine metabolic differences that exist
between normal proliferating cells and cancer cells. Cancer cells also exhibit significant alterations in the epigenome. Recent data indicate
that cellular metabolism and epigenetic phenomenon are engaged in crosstalk [1, 2]. Considering current efforts to target both cancer
metabolism and epigenetics, an understanding of the relationship between these two key features is of paramount importance [3, 4]. Here
we discuss the role of cellular metabolism in regulation of the epigenome. Moreover, we discuss how epigenetic changes may contribute
to establish cancer-specific metabolic features.
Keywords: Epigenetics, DNA methylation, histone modification, cancer metabolism, therapeutic targeting, glycolysis, TCA cycle, mitochondrial
oxidative phosphorylation, enzyme catalysis.
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