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Stem cells

The promises and perils of p53

Nature volume 460, pages 1085–1086 (2009)Cite this article

Five studies show that disabling p53, an essential tumour-suppressor protein, improves the efficiency of stem-cell production. Are these results a 'heads up' that cancer cells and stem cells are disturbingly similar?

Mutations that inactivate the p53 tumour-suppressor-protein network occur in most human cancers and, consequently, the roles and regulation of p53 activity in tumour formation are the topic of intense research. Inherited germline mutations in the p53 gene promote cancer in mice and humans, and p53 loss interacts with various mutant genes to transform normal cells into tumour cells. p53 is a stress-response protein, which suppresses tumour formation by triggering programmed cell death (apoptosis); by activating cell-cycle checkpoints that prevent damaged cells from proliferating; or by promoting senescence (permanent cell-cycle arrest). Thus, inactivation of p53 facilitates the expansion of aberrant cells and leads to rampant genome instability. Five papers1,2,3,4,5 in this issue describe how disruption of the p53 network also enhances the production of induced pluripotent stem (iPS) cellsFootnote 1. Although these observations catapult p53 into the centre of stem-cell research, time will tell whether they represent a promise or a warning.

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Figure 1: Overlapping mechanisms control iPS-cell and cancer-cell production.

Notes

  1. *This article and the papers concerned1,2,3,4,5 were were previously published online.

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  1. Valery Krizhanovsky and Scott W. Lowe are in the Cold Spring Harbor Laboratory and Howard Hughes Medical Institute, Cold Spring Harbor, New York 11724, USA.,

    Valery Krizhanovsky & Scott W. Lowe

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  1. Valery Krizhanovsky
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  2. Scott W. Lowe
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Krizhanovsky, V., Lowe, S. The promises and perils of p53. Nature 460, 1085–1086 (2009). https://doi.org/10.1038/4601085a

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