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Fig. 1 | Cancer & Metabolism

Fig. 1

From: Breast cancer cells that preferentially metastasize to lung or bone are more glycolytic, synthesize serine at greater rates, and consume less ATP and NADPH than parent MDA-MB-231 cells

Fig. 1

Tumor metabolism fluxes considered, except for those of the folate cycle. Red arrows: fluxes measured by extracellular substrate depletion (J0, J10a+10b, JRR) or product accumulation (J4, J22); purple arrows: fluxes measured by changes in glucose and/or glutamine consumption with pharmacological inhibitors (C75 for J13 and BSO for J18); blue arrows: inferred fluxes from 13C enrichment in lactate and/or serine (M-M3) from [1,2-13C] glucose or [5-13C] glutamine. Abbreviations: J0—glucose uptake/phosphorylation producing hexose phosphates (HxP), J1—oxidative pentose phosphate pathway (PPP) producing ribulose-5-phosphate (Ri5P) and NADPH, J2a—upper glycolysis producing triose phosphates (TrP: dihydroxyacetone phosphate and glyceraldehyde-3-phosphate), J2b—middle glycolysis producing 3-phosphoglycerate (3PG), ATP, and NADH, J2c—lower glycolysis producing pyruvate (Pyr) and ATP, J3f—forward non-oxidative PPP producing HxP and TrP, J3r—reverse non-oxidative PPP producing Ri5P, J4—lactate (Lac) production/export, J5—mitochondrial Pyr oxidation, J6a—mitochondrial oxidation of glycolytic NADH, J6b—oxidation of glycolytic NADH by other reactions, J7—cytoplasmic malic enzyme oxidation of malate (Mal), producing Pyr and NADPH (not shown), J8—NADPH consumption for ROS defense and biosynthesis, J9—Ri5P consumption for nucleotide synthesis, J10a—matrix glutamate (Glu) from glutamine (Gln) for glutathione (GSH) synthesis and glutamate dehydrogenase (GDH), J10b—Gln consumption by other reactions, J11a—GDH producing matrix α-ketoglutarate (αKG) and NADH, J11b—αKG from serine synthesis for the TCA cycle, J12f—citrate (Cit) oxidation and NADH/αKG production, J12r—NADPH-dependent reductive carboxylation of αKG for fatty acid (FA) synthesis, J13—FA synthesis from Cit, also yielding oxaloacetate (OAA; not shown), J14—αKG oxidation and NADH/succinyl CoA (SucC) production, J15—SucC oxidation yielding FADH2 and Mal, J16—Mal oxidation yielding NADH/OAA, J17—Cit synthesis from OAA and Pyr, J18—GSH synthesis from exogenous glutamine, J19—serine (SerICF) synthesis from 3PG, J20—endogenous serine (Serend) from sources other than 3PG contributing to the Ser pool, J21—Ser for the folate cycle, J22—Ser export to the extracellular fluid (ECF), and Red. Equiv.—mitochondrial NADH/FADH2

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