Oncogene-induced cellular senescence elicits an anti-Warburg effect.
Oncogene-induced senescence is now recognized as being an important mechanism in protecting against cancer. The phenotypic consequences, i.e., the inhibition of cell proliferation, are well described in model systems and specific events/key players defined. However, there is still the need to understand, at a more global level, the network of events involved both in terms of cause and consequence. This paper shows the power of systematic proteomic analyses, both targeted and global, in addressing such biological questions, highlighting the widespread nature of histone acetylation changes, and the opposite metabolic changes to those seen in the Warburg effect.
Clinical and Biomedical Proteomics Group, Leeds Institute of Cancer and Pathology, University of Leeds, Leeds, UK.
Rosamonde E
RE
Banks
D016922:Cellular Senescence / Q000235:genetics*; D006019:Glycolysis / Q000502:physiology*; D006657:Histones / Q000378:metabolism*; D006801:Humans; D024101:Mitochondrial Proteins / Q000096:biosynthesis*; D009369:Neoplasms / Q000378:metabolism*; D009857:Oncogenes; D040901:Proteomics / Q000379:methods*; D018631:ras Proteins / Q000235:genetics*
D006657:Histones; D024101:Mitochondrial Proteins; D018631:ras Proteins
Histones; Oncogene-induced senescence; Pyruvate dehydrogenase; Systems biology; Warburg effect