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. 2020 Sep 10;11(9):736. doi: 10.1038/s41419-020-02936-6

Fig. 5. Fatty acids activate PPARδ to promote CPT1A expression and Wnt signaling in colon cancer cells.

Fig. 5

a PT130 cells were treated with PPARδ agonist GW501516 (1 μM) for 24 h. The expression of CPT1A and PPARGC1A was determined using RT-PCR. Data represent the mean ± SD (n = 3, p < 0.0001). b Apc/Kras tumor organoids were treated with PPARδ agonist GW501516 (1 μM) for 48 h. The expression of Cpt1a and Ppargc1a was determined using RT-PCR. Data represent the mean ± SD (n = 3, *p < 0.01 and §p < 0.001). c PT130 cells were treated with OA alone or in combination with PPARδ antagonist GSK3787 (1 μM) for 24 h. The expression of CPT1A was determined using RT-PCR. Data represent the mean ± SD (n = 3, #p < 0.05,§p < 0.001, and p < 0.0001). d PT130 cells were treated with PA alone or in combination with PPARδ antagonist GSK3787 (1 μM) for 24 h. The expression of CPT1A and PPARGC1A was determined using RT-PCR. Data represent the mean ± SD (n = 3, §p < 0.001 and p < 0.0001). e Apc/Kras tumor organoids were treated with OA alone or in combination with PPARδ antagonist GSK3787 (1 μM) for 48 h. The expression of Cpt1a, Ppargc1a, and Wnt/β-catenin target genes (including Lgr5, Myc, and Axin 2) was determined using RT-PCR. Data represent the mean ± SD (n = 3, #p < 0.05, *p < 0.01, §p < 0.001, and p < 0.0001).