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Oncogene-like induction of cellular invasion from centrosome amplification

Author

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  • Susana A. Godinho

    (Howard Hughes Medical Institute, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children’s Hospital
    Harvard Medical School
    Present addresses: Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.).)

  • Remigio Picone

    (Howard Hughes Medical Institute, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children’s Hospital
    Harvard Medical School)

  • Mithila Burute

    (Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France
    Hôpital Saint Louis, Institut Universitaire d’Hematologie, U1160 INSERM/AP-HP/Université Paris Diderot, Paris 75010, France
    CYTOO SA, Grenoble 38054, France)

  • Regina Dagher

    (Howard Hughes Medical Institute, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children’s Hospital
    Harvard Medical School)

  • Ying Su

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Cheuk T. Leung

    (Harvard Medical School
    Present addresses: Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.).)

  • Kornelia Polyak

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Joan S. Brugge

    (Harvard Medical School)

  • Manuel Théry

    (Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France
    Hôpital Saint Louis, Institut Universitaire d’Hematologie, U1160 INSERM/AP-HP/Université Paris Diderot, Paris 75010, France)

  • David Pellman

    (Howard Hughes Medical Institute, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children’s Hospital
    Harvard Medical School)

Abstract

Cancer cells often have extra centrosomes, a paradox considering the detrimental effect extra centrosomes usually have on cell division; a study of human cells reveals that extra centrosomes can promote cancer cell invasion phenotypes through a pathway involving increased microtubule nucleation and Rac1 activity.

Suggested Citation

  • Susana A. Godinho & Remigio Picone & Mithila Burute & Regina Dagher & Ying Su & Cheuk T. Leung & Kornelia Polyak & Joan S. Brugge & Manuel Théry & David Pellman, 2014. "Oncogene-like induction of cellular invasion from centrosome amplification," Nature, Nature, vol. 510(7503), pages 167-171, June.
    • Handle: RePEc:nat:nature:v:510:y:2014:i:7503:d:10.1038_nature13277
    DOI: 10.1038/nature13277
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    Citations

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    Cited by:

    1. Marina A. Schapfl & Gina M. LoMastro & Vincent Z. Braun & Maretoshi Hirai & Michelle S. Levine & Eva Kiermaier & Verena Labi & Andrew J. Holland & Andreas Villunger, 2024. "Centrioles are frequently amplified in early B cell development but dispensable for humoral immunity," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    2. Carolin M. Sauer & James A. Hall & Dominique-Laurent Couturier & Thomas Bradley & Anna M. Piskorz & Jacob Griffiths & Ashley Sawle & Matthew D. Eldridge & Philip Smith & Karen Hosking & Marika A. V. R, 2023. "Molecular landscape and functional characterization of centrosome amplification in ovarian cancer," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    3. Bernardo P de Almeida & André F Vieira & Joana Paredes & Mónica Bettencourt-Dias & Nuno L Barbosa-Morais, 2019. "Pan-cancer association of a centrosome amplification gene expression signature with genomic alterations and clinical outcome," PLOS Computational Biology, Public Library of Science, vol. 15(3), pages 1-31, March.
    4. Revati Darp & Marc A. Vittoria & Neil J. Ganem & Craig J. Ceol, 2022. "Oncogenic BRAF induces whole-genome doubling through suppression of cytokinesis," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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