Fig. 3

The ERRα and p53 complex promotes mitochondrial function. a Cell viability was assessed by using crystal violet staining in CCD-18Co colon fibroblasts and a panel of colon cancer cell lines (Lim1215, HCT-116^p53+/+, HCT-116^p53−/−, HT-29, DLD-1, HCT-15, SW480, WiDr, and Caco-2). b IB analysis was performed using anti-ERRα, anti-ERRγ, anti-ERα, anti-p53 (low and high membrane exposition), and anti-GAPDH in CCD-18Co colon fibroblasts and a panel of colon cancer cell lines (Lim1215, HCT-116^p53+/+, HCT-116^p53−/−, HT-29, DLD-1, and HCT-15). c The cytosolic, membrane/organelle, and nuclear fractions were purified from XCT790-treated and untreated HCT-116^p53+/+ and HCT-116^p53−/− cells, and then IB analysis was performed using anti-ERRα, anti-p53, anti-VDAC1, anti-LaminB, and anti-α-Tubulin. d Venn diagram analysis examining the proteomic profile of the membrane/organelle fraction within three different comparisons: ii/i (no ERRα), iii/i (no p53), and iv/i (no ERRα/p53) as identified by mass spectrometry (n = 3 biological replicates per group). The bioinformatics tool found at http://bioinformatics.psb.ugent.be/webtools/Venn/ was used to generate the Venn diagram analysis. e Enriched KEGG pathways upregulated and downregulated obtained by STRING analysis of the membrane/organelle fraction comparing (iv) the absence of ERRα and p53 with the (i) presence of ERRα and p53. Comparisons between groups were made using multiple t tests with a false discovery rate of p ≤ 0.01. All cells were treated for 48 h with XCT790 (15 μM) or vehicle (DMSO). The data are shown as means ± S.D. (n = 3). The p value was calculated using a two-tailed Student’s t test. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; n.s., not significant