title: Engaging the p53 metabolic brake drives senescence.
abstract: Emerging evidence suggests that the ability of p53 to regulate metabolism is important for its tumor suppressor activity. A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression.
authors.affiliation: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
authors.forename: Dadi
authors.initials: D
authors.lastname: Jiang
authors.forename: Laura D
authors.initials: LD
authors.lastname: Attardi
mesh_terms: D017209:Apoptosis; D045744:Cell Line, Tumor; D016922:Cellular Senescence / Q000502:physiology*; D006801:Humans; D008291:Malate Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D009249:NADP / Q000378:metabolism; D051736:Proto-Oncogene Proteins c-mdm2 / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D016159:Tumor Suppressor Protein p53; D009249:NADP; D008291:Malate Dehydrogenase; C495394:malic enzyme 2; human; C497206:MDM2 protein, human; D051736:Proto-Oncogene Proteins c-mdm2