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LGALS3BP regulates centriole biogenesis and centrosome hypertrophy in cancer cells

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  • Marie-Laure Fogeron

    (Max-Planck Institute for Molecular Genetics
    Present address: Université Lyon 1, Univ Lyon, CNRS, UMR 5086, Bases Moléculaires et Structurales des Systèmes Infectieux, IBCP 7 passage du Vercors, F-69367, France)

  • Hannah Müller

    (Max-Planck Institute for Molecular Genetics)

  • Sophia Schade

    (Max-Planck Institute for Molecular Genetics)

  • Felix Dreher

    (Max-Planck Institute for Molecular Genetics)

  • Verena Lehmann

    (Max-Planck Institute for Molecular Genetics)

  • Anne Kühnel

    (Max-Planck Institute for Molecular Genetics)

  • Anne-Kathrin Scholz

    (Max-Planck Institute for Molecular Genetics)

  • Karl Kashofer

    (Institute of Pathology, Medical University of Graz)

  • Alexandra Zerck

    (Max-Planck Institute for Molecular Genetics)

  • Beatrix Fauler

    (Max-Planck Institute for Molecular Genetics)

  • Rudi Lurz

    (Max-Planck Institute for Molecular Genetics)

  • Ralf Herwig

    (Max-Planck Institute for Molecular Genetics)

  • Kurt Zatloukal

    (Institute of Pathology, Medical University of Graz)

  • Hans Lehrach

    (Max-Planck Institute for Molecular Genetics)

  • Johan Gobom

    (Max-Planck Institute for Molecular Genetics
    Present address: Department of Neuroscience and Physiology, University of Gothenburg, 43180 Mölndal, Sweden)

  • Eckhard Nordhoff

    (Max-Planck Institute for Molecular Genetics
    Present address: Department of Medicine, Center for Clinical Research I, Ruhr-University Bochum, Bochum 44801, Germany)

  • Bodo M.H. Lange

    (Max-Planck Institute for Molecular Genetics
    Alacris Theranostics GmbH)

Abstract

Centrosome morphology and number are frequently deregulated in cancer cells. Here, to identify factors that are functionally relevant for centrosome abnormalities in cancer cells, we established a protein-interaction network around 23 centrosomal and cell-cycle regulatory proteins, selecting the interacting proteins that are deregulated in cancer for further studies. One of these components, LGALS3BP, is a centriole- and basal body-associated protein with a dual role, triggering centrosome hypertrophy when overexpressed and causing accumulation of centriolar substructures when downregulated. The cancer cell line SK-BR-3 that overexpresses LGALS3BP exhibits hypertrophic centrosomes, whereas in seminoma tissues with low expression of LGALS3BP, supernumerary centriole-like structures are present. Centrosome hypertrophy is reversed by depleting LGALS3BP in cells endogenously overexpressing this protein, supporting a direct role in centrosome aberration. We propose that LGALS3BP suppresses assembly of centriolar substructures, and when depleted, causes accumulation of centriolar complexes comprising CPAP, acetylated tubulin and centrin.

Suggested Citation

  • Marie-Laure Fogeron & Hannah Müller & Sophia Schade & Felix Dreher & Verena Lehmann & Anne Kühnel & Anne-Kathrin Scholz & Karl Kashofer & Alexandra Zerck & Beatrix Fauler & Rudi Lurz & Ralf Herwig & K, 2013. "LGALS3BP regulates centriole biogenesis and centrosome hypertrophy in cancer cells," Nature Communications, Nature, vol. 4(1), pages 1-14, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2517
    DOI: 10.1038/ncomms2517
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    Cited by:

    1. Christina Kyrousi & Adam C. O’Neill & Agnieska Brazovskaja & Zhisong He & Pavel Kielkowski & Laure Coquand & Rossella Giaimo & Pierpaolo D’ Andrea & Alexander Belka & Andrea Forero Echeverry & Davide , 2021. "Extracellular LGALS3BP regulates neural progenitor position and relates to human cortical complexity," Nature Communications, Nature, vol. 12(1), pages 1-22, December.

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