Fig. 6

XCT790 attenuates the growth of PDX tumors in mice. a Direct DNA sequencing of the complete p53 genomic locus was performed for 37 samples of PDX colon cancers. Highlighted in the box are the point mutation detected in p53 and the number of mutated patient samples. b HCT-116^p53+/+ and HCT-116^p53_72R cell growth was analyzed. HCT-116^p53_72R cells were stably transduced with lentiviral constructs expressing mutant p53^72R fused to EGFP/luciferase, and HCT-116^p53+/+ cells were stably transduced with lentiviral control construct expressing EGFP/luciferase. HCT-116^p53+/+ and HCT-116^p53−/− cells were treated with XCT790 (15 μM) or vehicle (DMSO). c Body weight of mice was plotted over 25 days. d Growth of HJG172 PDX tumors was monitored for the entire duration of the experiment. Data represent means ± SEM. An unpaired t test was used to determine statistical significance; *P < 0.05. Images show the tumor xenografts dissected at the end of the experiments. e At the end of the treatment period, all animals were euthanized, and tumors were extracted and weighed. Data represent mean ± SEM. An unpaired t test was used to determine statistical significance; *P < 0.05. f Proposed model illustrating how the ERRα/p53 complex modulates mitochondrial biogenesis and function in colon cancer. Targeting ERRα in p53-deficient cells decreased the mtDNA copy number and mtOxPhos activity leading to an increased production of mitochondrial and intracellular ROS. XCT790 might be considered a potential drug to treat colon cancer patients