LGALS3BP regulates centriole biogenesis and centrosome hypertrophy in cancer cells

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, Kurt Zatloukal, Hans Lehrach, Johan Gobom, Eckhard Nordhoff and Bodo M.H. Lange ()
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Marie-Laure Fogeron: Max-Planck Institute for Molecular Genetics
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
Eckhard Nordhoff: Max-Planck Institute for Molecular Genetics
Bodo M.H. Lange: Max-Planck Institute for Molecular Genetics

Nature Communications, 2013, vol. 4, issue 1, 1-14

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms2517

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