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Tumour suppressors

The dark side of p27

Nature Reviews Cancer volume 7, page 637 (2007)Cite this article

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To study p27 function independent of its cell-cycle regulatory activity, the authors generated a knock-in mouse expressing a p27 mutant (p27CK−) in which four amino-acid replacements impair its ability to bind and inhibit cyclin–cyclin-dependent kinase (CDK) complexes. Similar to p27-null mice, p27CK−/CK− mice have an increased body size and organomegaly, features that underline the importance of p27 in cell-cycle regulation. But in contrast to p27-null mice, which only develop pituitary tumours, p27CK−/CK− mice (from two different genetic backgrounds) had a high incidence of hyperplastic lesions and spontaneous tumours in multiple tissues. Most mutant mice developed pituitary tumours, which were larger, more vascularized and more aggressive than those previously observed in p27-null mice, and caused death at an earlier age.

The oncogenic effect of the p27CK− mutant is genetically dominant given that p27+/CK− heterozygous mice develop hyperplastic and neoplastic lesions — although with a delayed onset compared with p27CK−/CK− homozygous mice — and genotyping of eight lung tumours from p27+/CK− mice did not show loss of heterozigosity in the wild-type allele.

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ORIGINAL RESEARCH PAPER

  1. Besson, A. et al. Discovery of an oncogenic activity in p27Kip1 that causes stem cell expansion and a multiple tumour phenotype. Genes Dev. 21, 1731–1746 (2007)

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Authors
  1. Francesca Pentimalli
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Pentimalli, F. The dark side of p27. Nat Rev Cancer 7, 637 (2007). https://doi.org/10.1038/nrc2216

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  • DOI: https://doi.org/10.1038/nrc2216

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