Cytoplasmic functions of the tumour suppressor p53

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Abstract
The p53 tumour suppressor is inactivated by mutation in about half of all human cancers, and in many of the remainder the p53 pathway is inhibited in some way. p53 has been much studied of course, but mainly as a transcription factor and gene regulator. Douglas Green and Guido Kroemer present a review of an emerging area of p53 research, its role in the cytosol, where it triggers apoptosis and inhibits autophagy. These extranuclear actions — unknown until recently — contribute to p53's efficacy as a tumour suppressor, and may offer new targets for modulation of the p53 system. The principal tumour-suppressor protein, p53, accumulates in cells in response to DNA damage, oncogene activation and other stresses. It acts as a nuclear transcription factor that transactivates genes involved in apoptosis, cell cycle regulation and numerous other processes. An emerging area of research unravels additional activities of p53 in the cytoplasm, where it triggers apoptosis and inhibits autophagy. These previously unknown functions contribute to the mission of p53 as a tumour suppressor.