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. 2018 Jan 2;14(1):e1005914. doi: 10.1371/journal.pcbi.1005914

Fig 2. Differences in LCFA metabolism activity between the PC-3/M and PC-3/S cells.

Fig 2

A: Computational analysis predicts long chain fatty acid transport (LCFA) from cytosol into the mitochondria via CPT1 and LCFA β-oxidation to be more active in PC-3/M cells. B: PC-3/M cells show a higher sensitivity to CPT1 inhibition. Validation of model predictions by measuring Oxygen consumption rate (OCR) before and after inhibition of CPT1 with etomoxir. Measurement values were normalized to pre-inhibition OCR values. Green line, OCR associated with PC-3/S cells; blue line, OCR associated with PC-3/M cells (mean value of three replicates). The end-point values are represented as means ± SD. p-value < 0.001, calculated using Mann-Whitney U test. C: PC-3/M cells present higher levels of CPT1 protein. Validation of model prediction by measuring CPT1 protein levels by western blotting. β-Actin levels were used as a protein loading and transfer control. On the right, quantification of western blot by using ImageJ software [33]. D: The concentration of DHA, a LCFA with anti-proliferative properties, is significantly higher in PC-3/S cells (p-value < 0.05 calculated with one tail Mann-Whitney U test). Values represent means ± sd of three replicates. PC-3/S: 3143.38 ± 857.98 fmol/10^6 cells; PC-3/M: 1195.91 ± 219.19 fmol/10^6 cells. E: PC-3/M cells present significantly higher levels of acylcarnitines (p-value < 0.001). F: Dose-effect relationship between the antiproliferative effects of etomoxir and cell proliferation in PC-3/M and PC-3/S subpopulations and parental PC-3 cells.