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. 2017 Dec 20;7:313. doi: 10.3389/fonc.2017.00313

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Copyright © 2017 Ždralević, Marchiq, de Padua, Parks and Pouysségur.

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) or licensor 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 reprogramming in glucose-6-phosphate isomerase (GPI)-KO cells. A switch from glycolytic metabolism to oxidative phosphorylation (OXPHOS) caused by the complete GPI disruption is shown. LS174T WT cells are highly glycolytic and do not use mitochondria for ATP production (A). Contrarily, cells survive GPI disruption by re-activating pentose phosphate pathway (PPP) and OXPHOS (B). Oxygen consumption rate (OCR) of LS174T WT and GPI-KO cells was evaluated with Seahorse XF24 bioanalyzer (C). The mean ± SEM is representative of four independent experiments performed in quadruplicate. The figure is adapted from Ref. (39). Glc, glucose, oligo, oligomycin, FCCP, carbonyl cyanide-4-(trifluoromethoxy) phenylhydrazone, rot, rotenone, antA, antimycin A.