Abstract
Cancer cells feature strong metabolic changes to cope with the high energy demand for cell growth and division. Given the importance of metabolic reprogramming in tumor development, it seems logical that tumor suppressors and oncogenes are also regulating the molecular pathways controlling these processes. The p53 tumor suppressor gene has been extensively studied for its role in responding to DNA damage, hypoxia, and oncogenic activation. During the last years, we have learnt that p53 has also the capacity to modulate metabolic changes in cells by regulating a large variety of pathways such as glycolysis, oxidative phosphorylation or fatty acid metabolism. Our group has recently found that the lack of p53 in AgRP neurons, but not POMC neurons, causes that mice are more prone to develop diet-induced obesity (Nat Commun. 9(1):3432). The reason for this is that these mice showed a late increase in food intake and especially because they had a reduced thermogenic activity in BAT. The mechanism modulating these actions involves the upregulation of MKK7 that activates c-Jun N-terminal kinase.