Figure 7
From: Bioenergetic Adaptations in Chemoresistant Ovarian Cancer Cells
Cisplatin induces a highly active metabolic state in chemosensitive cells. A2780 chemosensitive cells were treated with a non-toxic low dose of cisplatin for 24 and 48 hours and then subjected to measurement of (A) ECAR profile after (1) glucose (fuel for glycolysis), (2) oligomycin (an ATP synthase blocker) and (3) 2DG (an inhibitor of glycolysis) injections (C) OCR profile measured under similar conditions after (1) oligomycin (ATP synthase inhibitor), (2) FCCP (an electron transport chain uncoupler) and (3) rotenone (an inhibitor of electron transport chain) injections. (B) Basal glycolysis and glycolytic capacity is increased by cisplatin exposure. (D) Basal mitochondrial respiration and maximum respiration is increased by cisplatin exposure. (E) OCR: ECAR ration indicate a shift in bioenergetics phenotype from glycolytic to highly active metabolism after cisplatin treatment. (F) Cisplatin (1 uM) is non-toxic at the concentration used. All Seahorse experiments were carried out in triplicates and replicated thrice. ***p < 0.001, **p < 0.01, NS: non-significant cisplatin treated compared to untreated. Abbreviations: ATP: adenosine triphosphatase; 2DG: 2-deoxyglucose; FCCP: carbonylcyanide-p-trifluoromethoxyphenyl hydrazine. OCR: Oxygen Consumption Rate; ECAR: Extracellular Acidification Rate.
