Plk1 overexpression induces chromosomal instability and suppresses tumor development View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-08-01

AUTHORS

Guillermo de Cárcer, Sharavan Vishaan Venkateswaran, Lorena Salgueiro, Aicha El Bakkali, Kalman Somogyi, Konstantina Rowald, Pablo Montañés, Manuel Sanclemente, Beatriz Escobar, Alba de Martino, Nicholas McGranahan, Marcos Malumbres, Rocío Sotillo

ABSTRACT

Polo-like kinase 1 (Plk1) is overexpressed in a wide spectrum of human tumors, being frequently considered as an oncogene and an attractive cancer target. However, its contribution to tumor development is unclear. Using a new inducible knock-in mouse model we report here that Plk1 overexpression results in abnormal chromosome segregation and cytokinesis, generating polyploid cells with reduced proliferative potential. Mechanistically, these cytokinesis defects correlate with defective loading of Cep55 and ESCRT complexes to the abscission bridge, in a Plk1 kinase-dependent manner. In vivo, Plk1 overexpression prevents the development of Kras-induced and Her2-induced mammary gland tumors, in the presence of increased rates of chromosome instability. In patients, Plk1 overexpression correlates with improved survival in specific breast cancer subtypes. Therefore, despite the therapeutic benefits of inhibiting Plk1 due to its essential role in tumor cell cycles, Plk1 overexpression has tumor-suppressive properties by perturbing mitotic progression and cytokinesis. More... »

PAGES

3012

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-018-05429-5

    DOI

    http://dx.doi.org/10.1038/s41467-018-05429-5

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1105858674

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30069007


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