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. 2018 Nov 2;8:500. doi: 10.3389/fonc.2018.00500

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Copyright © 2018 Zaal and Berkers.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Metabolic pathways involved in anticancer drug resistance in multiple myeloma (A), lung- and ovarian cancer (B), breast cancer (C), and melanoma (D). Metabolic enzymes that are associated with drug resistance are shown in purple. Metabolic inhibitors that can be used to target drug-resistant cancers are depicted in red. 2-DG, 2-deoxyglucose; 2ME, 2-methoxyestradiol; 6-AN, 6-aminonicotinamide; ATP, adenosine triphosphate; BPTES, bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide; BSO, buthionine sulphoximine; FASN, fatty acid synthase; G6PDH, glucose-6-phosphate dehydrogenase; GCLC, glutamate-cysteine ligase; GLS, glutaminase; HK2, hexokinase 2; I, complex I; II, complex II; III, complex III; IV, complex IV; LDHA, lactate dehydrogenase A; LDHB, lactate dehydrogenase B; mTOR, mammalian target of rapamycin; NQO1, NAD(P)H quinone dehydrogenase; PDH, pyruvate dehydrogenase complex; PDK1, pyruvate dehydrogenase kinase 1; PHGDH, 3-phosphoglycerate dehydrogenase; PPP, pentose phosphate pathway; R5P, ribose 5-phosphate; ROS, reactive oxygen species; SOD2, superoxide dismutase 2; SSP, serine synthesis pathway; TCA, tricarboxylic acid cycle; V, complex V; xCT, glutamate/cysteine xCT antiporter.