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. Author manuscript; available in PMC: 2024 Oct 17.
Published in final edited form as: Mol Cancer Res. 2021 Jun 25;19(9):1534–1545. doi: 10.1158/1541-7786.MCR-20-0991

Fig 5. APJ pathway promotes fatty acid utilization in OvCa cells.

Fig 5.

(A) Fuel dependency for oxidation of glucose, glutamine, and fatty acids in OVCAR-5-EV and APJ cells as quantified by Seahorse Metabolic Analyzer. (B) Fuel flexibility for oxidation of glucose, glutamine, and fatty acids in OVCAR-5-EV and APJ cells. (C,D) Oxygen consumption rate (OCR) in OVCAR-5-EV and APJ cells when treated with (C) BSA and palmitate, and (D) BSA and palmitate in presence of CPT1a inhibitor etomoxir (40 μM) as quantified by Seahorse Metabolic Analyzer. Quantification of (E) Basal respiration rates, (F) Mitochondrial ATP production rate (oligomycin [oligo]-sensitive respiration), and (G) Maximal respiration rate (induced by FCCP, uncoupler of mitochondrial oxidative phosphorylation [OXPHOS]) in OVCAR-5-APJ cells in presence of etomoxir (40 μM).

Results were obtained from 2 independent experiments (mean±SEM). Statistical analysis was performed using one-way ANOVA followed by Tukey post hoc test for A,B,E-G. *P< 0.05; **P< 0.01; ***P< 0.001; ****P<0.0001.