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. 2022 Sep 13;13:5371. doi: 10.1038/s41467-022-33138-7

Fig. 5. Inhibition of fatty acid transporter FATP1 abolishes fatty acid metabolic switch in CD37KO B-cell lymphoma.

Fig. 5

WT and CD37KO lymphoma cells (BJAB) were incubated in a nutrient-rich medium with or without FATP1 inhibitor (compound 5k (12.5 µM)) for 2 h. Cells were then transferred to a nutrient-restricted medium with (n = 8) or without (n = 8) compound 5k and subjected to an acute substrate injection of medium or palmitate (50 µM) (a) or oleic acid (50 µM) (d) at t = 30 min. Continuous oxygen consumption ratio (OCR) values are shown in response to FCCP (1 µM) at t = 70 min and Rotenone/AntimycinA (Rot/AA) (1 µM) at t = 100 min. Substrate-induced OCR (b, e) were calculated as the difference between baseline and acute substrate injection (b: p = 0.0099). The spare respiratory capacity (SRC) (c, f) was calculated as the difference in OCR between baseline and FCCP (c: WT vs KO; p = 0.0365, KO vs KO palmitate; p = 0.0188). Relative ATP production (counts per second, CPS) was assessed in response to 24-h FATP1 inhibition with compound 5k (12.5 µM) (n = 3, WT− vs KO−; p = 0.0008, KO− vs KO+; p = 0.0003) (g). Decrease in palmitate uptake was measured after 2 h FATP1 inhibition with compound 5k (n = 6, WT; p = 0.0147, KO; p = 0.0033) (h) and 12a (n = 6, KO; p = 0.0355, p = 0.0315) (i) and compared to non-treated cells (n = 6). Experiments were repeated three times, yielding similar results. Two-way ANOVA with Tukey’s post hoc test were performed to check for significant differences between the indicated groups, ns not significant *p < 0.05, **p < 0.01, ***p < 0.001 ****p < 0.0001. Error bars represent mean ± SD. Source data are provided as a Source Data file. See also Supplementary Fig. 5.