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. Author manuscript; available in PMC: 2012 Apr 26.
Published in final edited form as: Cell. 2012 Mar 16;148(6):1132–1144. doi: 10.1016/j.cell.2012.02.032

Figure 3. Cancer cell metabolism.

Figure 3

(A) Cancer cells rely primarily on glucose and glutamine to supply intermediary metabolism. Several metabolite pools fed by these nutrients and thought to be essential for tumor cell growth are highlighted in yellow. Uptake and catabolism of glucose and glutamine is regulated by oncogenic signaling. Suspected metabolic tumor suppressors (red) and oncogenes (green) control the abundance of a handful of key metabolites (bold) that regulate additional signaling functions as described in the text. These signaling activities likely contribute to malignant transformation or the propagation of growth signals within transformed cells. Thus, in addition to their traditional roles in metabolism, FH, SDH and the 2-HG dehydrogenases serve to suppress levels of pro-oncogenic metabolites. 2SC, S-(2-succinyl)-cysteine.

(B) Detailed view of selected metabolites and enzymes discussed in the text. Abbreviations: Aco, aconitase; IDH, isocitrate dehydrogenase; αKGDH, α-ketoglutarate dehydrogenase; SCS, succinyl-CoA synthetase; SDH, succinate dehydrogenase; FH, fumarate hydratase; mut IDH1/IDH2, mutant isocitrate dehydrogenase 1 or 2; (D)-2HG DH; (D)-2-hydroxyglutaric acid dehydrogenase.