Plk4 haploinsufficiency causes mitotic infidelity and carcinogenesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-07-17

AUTHORS

Michael A Ko, Carla O Rosario, John W Hudson, Sarang Kulkarni, Aaron Pollett, James W Dennis, Carol J Swallow

ABSTRACT

The polo-like kinase Plk4 (also called Sak) is required for late mitotic progression, cell survival and postgastrulation embryonic development1. Here we identified a phenotype resulting from Plk4 haploinsufficiency in Plk4 heterozygous cells and mice. Plk4+/− embryonic fibroblasts had increased centrosomal amplification, multipolar spindle formation and aneuploidy compared with wild-type cells. The incidence of spontaneous liver and lung cancers was ∼15 times high in elderly Plk4+/− mice than in Plk4+/+ littermates. Using the in vivo model of partial hepatectomy to induce synchronous cell cycle entry, we determined that the precise regulation of cyclins D1, E and B1 and of Cdk1 was impaired in Plk4+/− regenerating liver, and p53 activation and p21 and BubR1 expression were suppressed. These defects were associated with progressive cell cycle delays, increased spindle irregularities and accelerated hepatocellular carcinogenesis in Plk4+/− mice. Loss of heterozygosity occurs frequently (∼60%) at polymorphic markers adjacent to the PLK4 locus in human hepatoma. Reduced Plk4 gene dosage increases the probability of mitotic errors and cancer development. More... »

PAGES

883-888

Journal

TITLE

Nature Genetics

ISSUE

8

VOLUME

37

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng1605

DOI

http://dx.doi.org/10.1038/ng1605

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008610787

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16025114


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